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HEMODYNAMIC MONITORING

Hemodynamic is the term used to describe the intravascular pressure and flow that occurs when the heart muscle contracts and pumps blood throughout the body. It is important to remember that the vascular system is a closed circuit. Pressure and flow variations in the venous compartment will necessarily affect the arterial compartment and vice versa. Therefore, a hemodynamic measurement is not simply a number in relation to a norm. Rather, it is the minute to minute pressure and flow variations that occur within and between compartments.

Heart function is the main focus of hemodynamic studies but the heart is not the only factor influencing pressure and flow. There are four factors which influence hemodynamics. They are the three hemodynamic components to the circulation of blood in the body plus chronotropy.

Intravascular volume: the amount of fluid circulating in the vasculature. This can be affected by dehydration, diuresis, and volume overload due to heart or kidney failure. Intropy: the strength of myocardial contractions. Myocytes are the only muscle cells which are able to vary the strength of contraction. Intropy can be affected by exercise, stress and pharmaceutical agents, which increase the strength of myocardial contractions, or by cardiac diseases such as heart failure, which decrease the strength of contractions.

Vasoactivity: the expanding and contracting of blood vessels to accommodate the variation in blood flow, regulate arterial pressure, and meet the metabolic demands of the organs and body tissues. Certain hormones also affect vasoactivity. They are angiotenson II, epinephrine, norepinephrine, and vasopressin. The fourth factor is chronotropy. Chronotropy involves the timing, or rate of heart contraction. This component affects tissue perfusion and is not considered a hemodynamic component. However, a person needs to have all four components functioning normally to remain hemodynamically stable.

HEMODYNAMIC MEASUREMENT TERMINOLOGY

PARAMETERS

Normal value Blood Pressure Systolic (SBP)90-140 mmHg Diastolic (DBP) 60-90mmHg Mean Arterial Pressure (MAP) 70 - 100 mm Hg Cardiac Index (CI) 2.5-4 L/min/m2 Cardiac Output (CO) 4-8 L/min Central Venous Pressure (CVP) (also known as Right Atrial Pressure (RA)) 2-6 mmHg Pulmonary Artery Pressure (PA) Systolic 20-30 mmHg (PAS) Diastolic 8-12 mmHg (PAD) Mean 25 mmHg (PAM)

Pulmonary Vascular Resistance (PVR) 37-250 dynes/sec/cm5 Right Ventricular Pressure (RV) Systolic-20-30 mmHg Diastolic 0-5 mmHg Stroke Index (SI) 25 - 45 ml/m2 Stroke Volume (SV) 50 - 100 ml Systemic Vascular Resistance (SVR) 800-1200 dynes/sec/cm5

Afterload: Afterload describes the resistance that the heart has to overcome, during every beat, to send blood into the aorta. These resistive forces include vasoactivity and blood viscosity. Cardiac Index (CI): The amount of blood pumped by the heart, per minute, per meter square of body surface area. Cardiac Output (CO): The volume of blood pumped by the heart in one minute.

Increased cardiac output may indicate a high circulating volume. Decreased cardiac output indicates a decrease in circulating volume or a decrease in the strength of ventricular contraction.

Central Venous Pressure (CVP): CVP readings are used to approximate the Right Ventricular End Diastolic Pressure (RVEDP). The RVEDP assesses right ventricular function and general fluid status.

Low CVP values typically reflect hypovolemia or decreased venous return. High CVP values reflect overhydration, increased venous return or right sided cardiac failure.

Mean Arterial Pressure (MAP): Reflects changes in the relationship between cardiac output (CO) and systemic vascular resistance (SVR) and reflects the arterial pressure in the vessels perfusing the organs.

A low MAP indicates decreased blood flow through the organs. A high MAP indicates an increased cardiac workload.

Preload: Preload occurs during diastole. It is the combination of pulmonary blood filling the atria and the stretching of myocardial fibers. Preload is regulated by the variability in intravascular volume.

Volume reduction decreases preload Volume increase will increase preload, mean arterial pressure (MAP) and stroke index (SI).

Pulmonary Artery Pressure (PA Pressure): Blood pressure in the pulmonary artery.

Increased pulmonary artery pressure may indicate: a left-to-right cardiac shunt, pulmonary artery hypertension, COPD or emphysema, pulmonary embolus, pulmonary edema, left ventricular failure.

Pulmonary Capillary Wedge Pressure (PCWP or PAWP): PCWP pressures are used to approximate LVEDP (left ventricular end diastolic pressure).

High PCWP may indicate left ventricle failure, mitral valve pathology, cardiac insufficiency, cardiac compression post hemorrhage.

Pulmonary Vascular Resistance (PVR): The measurement of resistance or the impediment of the pulmonary vascular bed to blood flow.

An increased PVR or "Pulmonary Hypertension" is caused by pulmonary vascular disease, pulmonary embolism, or pulmonary vasculitis, or hypoxia. A decreased PVR is caused by medications such as calcium channel blockers, aminophylline, or isoproterenol or by the delivery of O2.

Right Ventricular Pressure (RV Pressure): A direct measurement that indicates right ventricular function and general fluid status.

High RV pressure may indicate: pulmonary hypertension, right ventricle failure, congestive heart failure.

Stroke Index or Stroke Volume Index: (SI or SVI): The amount of blood ejected from the heart in one cardiac cycle, relative to Body Surface Area (BSA). It is measured in ml per meter square per beat.

An increased SVI may be indicative of early septic shock, hyperthermia, hypervolemia or be caused by medications such as dopamine, dobutamine, or digitalis. A decreased SVI may be caused by CHF, late septic shock, beta blockers, or an MI. A decreased SV may indicate impaired cardiac contractility or valve dysfunction and may result in heart failure. An increased SV may be caused by an increase in circulating volume or an increase in inotropy.

Stroke Volume (SV): The amount of blood pumped by the heart per cardiac cycle. It is measured in ml/beat.

Systemic Vascular Resistance (SVR): The measurement of resistance or impediment of the systemic vascular bed to blood flow.

An increased SVR can be caused by vasoconstrictors, hypovolemia, or late septic shock. A decreased SVR can be caused by early septic shock, vasodilators, morphine, nitrates, or hypercarbia.

NON INVASIVE HEMODYNAMIC ASSESSMENT

A patient's hemodynamic status can be evaluated noninvasively by performing a comprehensive cardiovascular assessment. This assessment should be conducted in addition to invasive monitoring.

Assessment Take vital signs: Assess pulse for rhythm, strength and rate. Assess blood pressure. Precordium: Inspect the anterior chest for heaves and an increase in visible pulsatility. Palpate the PMI (point of maximum impulse) for a normal 2+ pulse. Percuss the chest to determine the size of the heart. Auscultate the aortic, pulmonic, second pulmonic (Erb's point), mitral, and tricuspid areas of the precordium. Peripheral Vascular: Inspect and palpate the skin for color, texture, moisture and turgor. Palpate the peripheral pulses and check nailbed capillary refill which is normally less than 3 seconds. Inspect the neck for jugular venous distention (JVD). Auscultate and palpate the carotid arteries to assess arterial blood flow. Assess for hepatojugular reflux.

ARTERIAL BLOOD PRESSURE MONITORING

Intra-arterial catheters ("art lines") offer clinicians a low risk and reliable method to continuously monitor systemic blood pressure. Critically ill patients, with unstable cardiopulmonary status, often benefit from such continuous monitoring. Clinicians are better able to promptly manage changes in blood pressure which may signal perfusion deficits. A secondary benefit of an art line is the ability to do serial blood sampling. Arterial blood gas evaluations can be performed without the need for repeated painful needle sticks. Arterial blood gas monitoring is vital to the successful treatment of respiratory failure, whatever the cause. Arterial pressure monitoring begins with an accurate patient history and assessment. A history of peripheral vascular disease could raise the risk of complications from arterial line insertion. Skin changes, scars, sores, discoloration, swelling, excess warmth or swelling etc., could indicate the presence of peripheral vascular disease.

Palpation, capillary refill and the Allen test are necessary steps to determine the suitability of a limb for insertion of an arterial line. The Allen test determines the patency of the arm's radial and ulnar arteries. The Allen test must be done prior to arterial line insertion, in order to reduce the risk of ischemia due to arterial occlusion. Ask seated patient to place hand, palm up, on the knee. Using both of your thumbs, compress the radial and ulnar arteries. Ask patient to open and close a fist several times, watch for blanching of the palm. Release only the radial artery; palm should become pink in seconds. Repeat process this time releasing only the ulnar artery. If the palm remains blanched when either the radial or ulnar arteries are released, there may not be sufficient circulation if a catheter were to be inserted. Follow your institutional guidelines when inserting or assisting in the placement of an arterial line. The necessary equipment for placement will include: Skin cleansing supplies Positioning aides Sterile gloves Sterile angiocath Airless, sterile and flushed pressure tubing/ transducer assembly Sterile supplies to secure and dress the angiocath (sterile suture and scissors). Monitor once the catheter is inserted, it is connected to the flushed and airless tubing/transducer assembly. The transducer should be positioned level with the heart, then zeroed to negate the pressure applied by the heparinized flush. When zeroed, the transducer will reflect changes in the intra-arterial pressure.

Waveform evaluation is the best method to determine correct placement. A normal wave form will be: within normal blood pressure limits, present a characteristic shape and synch with the EKG waveform. Correlation of pressure readings with blood pressure cuff should be done periodically, if possible. The normal peripheral arterial waveform will display the peak systolic pressure after the QRS. This phenomenon reflects the time it takes the cardiac systolic pressure wave to reach the peripheral catheter and sensor. The dicrotic notch reflects the closure of the aortic valve. Of course, the same time delay applies to the dicrotic notch. The aortic valve has closed prior to the display of the notch. The time delay is a function of both distance and compliance or elasticity of the vessels. The waveform of a patient with arteriosclerotic disease would be steeper in ascent and descent, therefore shorter in duration and the notch would be less well defined.

CENTRAL VENOUS PRESSURE MONITORING

Central venous pressure is considered a direct measurement of the blood pressure in the right atrium and vena cava. It is acquired by threading a central venous catheter (subclavian double lumen central line shown) into any of several large veins. It is threaded so that the tip of the catheter rests in the lower third of the superior vena cava. The pressure monitoring assembly is attached to the distal port of a multilumen central vein catheter

ASSISTING WITH CVP PLACEMENT


Adhere to institutional Policy and Procedure. Obtain history and assess the patient. Explain the procedure to the patient, include:

local anesthetic trendelenberg positioning draping limit movement need to maintain sterile field. post procedure chest X-ray

Obtain a sterile, flushed and pressurized transducer assembly Obtain the catheter size, style and length ordered. Obtain supplies:

Masks Sterile gloves Line insertion kit Heparin flush per policy

Position patient supine on bed capable of trendelenberg position Prepare for post procedure chest X-ray

The CVP catheter is an important tool used to assess right ventricular function and systemic fluid status. Normal CVP is 2-6 mm Hg. CVP is elevated by :

overhydration which increases venous return heart failure or PA stenosis which limit venous outflow and lead to venous congestion positive pressure breathing, straining, hypovolemic shock from hemorrhage, fluid shift, dehydration negative pressure breathing which occurs when the patient demonstrates retractions or mechanical negative pressure which is sometimes used for high spinal cord injuries.

CVP decreases with:


The CVP catheter is also an important treatment tool which allows for: Rapid infusion Infusion of hypertonic solutions and medications that could damage veins Serial venous blood assessment

SITE CARE AND CATHETER SAFETY:

A sterile dressing is placed over the insertion site and the catheter is taped in place. The insertion site should be assessed for infection and the dressing changed every 72 hours and prn. The placement of the catheter, stated in centimeters, should be documented and assessed every shift. The integrity of the sterile sleeve must be maintained so the catheter can be advanced or pulled back without contamination. The catheter tubing should be labeled and all the connections secure. The balloon should always be deflated and the syringe closed and locked unless you are taking a PCWP measurement.

PATIENT ACTIVITY AND POSITIONING:


Many physicians allow stable patients who have PA catheters, such as post CABG patients, to get out of bed and sit. The nurse must position the patient in a manner that avoids dislodging the catheter. Proper positioning during hemodynamic readings will ensure accuracy.

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