Hemodynamics Is defined as the study of the forces involved in blood circulation. Hemodynamic monitoring is used to assess cardiovascular function in the critically ill or unstable client It is indicated when standard vital signs measurements are not adequate to evaluate changes in cardiovascular status.

Purpose The main goals of invasive hemodynamic monitoring are to evaluate cardiac function, the condition of the circulatory system, and the clients response to interventions Provide additional information which establishes or expands a given diagnosis Provides a physiological rationale for a selected therapy Allows a rapid determination of the response to therapy or suggest a change in the response

Types Intrarterial Blood Pressure Monitoring Central Venous Pressure Monitoring Pulmonary Artery Pressure Monitoring The hemodynamic pressures include heart rate, arterial blood pressure, central blood pressure, pulmonary pressures, and cardiac output

Direct versus Derived Parameters Direct hemodynamic parameters are obtained straight from the monitoring device for example the heart rate, and various pressures such as arterial and venous pressures Derived hemodynamic pressures are calculated using the direct hemodynamic data; they include such measurements such as cardiac index, mean arterial blood pressure (MAP), and stroke volume (SV)

Hemodynamic Monitoring Systems Measure the pressures within the vessel and converts this signal into an electrical waveform that is amplified and displayed The electrical signal may be graphically recorded on pressure graph paper and displayed numerically on the monitor System components include an invasive catheter threaded into artery or vein connected to a transducer by stiff high-pressure tubing

Hemodynamic Monitoring Systems The pressure transducer translates pressure measurements into an electrical signal that is in turn relayed to the monitor Additional components include stopcocks and a continuous flush system with heparinized saline and an infusion pressure bag to keep clots from forming in the catheter

Leveling the Transducer Is important to ensure accurate readings The point used as a constant reference is the level of the right atrium It is located by intersecting two imaginary lines: one drawn down the lateral chest wall from the clients 4th intercostal space, the other line is mid chest level (the midaxillary line) Once located, this junction is marked with ink or tape and used consistently for pressure readings

Cardiac and Vascular Structures

Function of the Heart To pump blood returning from the body to the lungs and into the Aorta Delivers oxygenated blood and nutrients to the tissue and removes metabolic waste products How well the heart performs its function is determined primarily by heart rate, preload, ventricular afterload, and ventricular contractility

Cardiac Cycle Refers to one complete mechanical cycle of the heartbeat, beginning with ventricular contraction (systole) and ending with ventricular relaxation (diastole) The amount of blood ejected from the ventricles with each contraction is called stroke volume

Ventricular Systole (contraction) The ventricles begin to tense causing a rise in pressure. When the ventricular pressure is greater than the atrial pressure, the mitral and tricuspid valves close. The closure of these valves causes the first heart sound S1 and marks the onset of systole Briefly, there is a stage of systole when all four valves are closed. Since there is no change in ventricular volume, this stage is called isovolumetric or isovolumic contraction Ventricular tension continues to increase, eventually exceeding aortic and pulmonary artery pressures. This causes the aortic and pulmonic valves to open

Ventricular Systole (contraction) Blood is rapidly ejected into the aorta and pulmonary artery, causing the rapid ejection phase of systole Deceleration of blood occurs, due to an increase in pressure in the aorta and pulmonary artery (the reduced ejection phase of systole). When aortic and pulmonary pressures exceed those of the ventricles, the aortic and pulmonic valves close. The closure of these valves causes the second heart sound and marks the end of systole

Ventricular Diastole (relaxation) Once again all four valves are briefly closed. Since all valvesare closed, ventricular volume does not change, therefore the first phase of diastole is called isovolumetric, or isovolumic relaxation As the ventricles relax, ventricular pressure decreases. When ventricular pressure is less than atrial pressure, the mitral and tricuspid vales open The ventricles fill with blood rapidly at first and then at a reduced rate. This state of filling is passive After the ventricles have filled passively, atrial systole occurs. Up to 30% of ventricular filling is contributed by atrial contraction. This may also be called atrial kick

Flow of Blood

Cardiac Output The performance of the heart as a pump is reflected by the cardiac output (CO) This is the volume of blood pumped per minute, 4-8 litres/min in the average adult at rest (or 4-6) The CO is equal to stroke volume X heart rate The healthy heart can augment HR & SV and greatly increase CO to meet O2 supply and demand. In the critically ill patient, the tissue demands are great and these normal mechanisms are often nonfunctional

Cardiac Output The normal cardiac output for individuals can vary significantly depending on body size A tall, heavy person needs more CO to feed all of his or her cells than does a short, light person. Because of this, when CO is measured, it should be corrected to account for body size

Cardiac Index The correction is calculated by dividing the CO by the body surface area (BSA) and it is called the cardiac index (CI) The normal CI is 2.5 to 4.5 L/min/m2 This is a more accurate indicator of cardiac function than cardiac output A minimum of 2.0 L/min/m2 is required to maintain life without mechanical support

Cardiac Output The BSA is calculated via the use of nomograms or computer programs from the patients height and weight For example, if two patients each have a CO of 5.0 L/min but one has a BSA of 1.0 m2 and the other has a BSA of 2.0 m2, their CIs (5.0 L/m2 and 2.5 L/m2, respectively) illustrate that the perfusion of tissue is quite different despite their equal COs

Cardiac Output Total blood volume is approx 5 litres, this means essentially all blood is pumped completely around the circuit once each minute During periods of exercise the CO may increase to 30 litres/min, this increase on CO reflects an increase in HR and/or SV

Heart Rate HR are primarily controlled via the parasympathetic and sympathetic branches of the ANS Sympathetic stimulation, the HR increases, with parasympathetic stimulation, the HR decreases In the resting state the parasympathetic influence is dominant and resting heart rate is 60-80 beats/min in the average adult Heart rate is also influenced by circulating catechlolamines, which increase heart rate Blood volume in the right atrium has a direct relationship with HR. This is known as the brainbridge reflex

Heart Rate When the need for and increased CO arises e.g. exercise, the HR increases abruptly, and may progressively increase CO by 2 – 3 times in the healthy individual In the critically ill patient, an increase HR, as a means of increasing CO, may be offset by its associated negative implications

Negative Implications As HR increases, myocardial oxygen demand increases AS diastolic time decreases, ventricular filling is less optimal, and cardiac output may decrease As diastolic time decreases, coronary artery filling decreases, the coronary artery perfusion decreases

Heart Rate A decrease in heart rate may result in an increase in CO in some patients As heart rate decreases, diastolic filling time increases, optimizing ventricular filling When heart rate alone cannot cause a increase in CO, stroke volume may compensate

Stroke Volume The second determinant of cardiac output is stroke volume, the volume of blood pumped with each heartbeat Stroke volume is calculated by dividing CO by heart rate. Normal SV is 60 – 100 ml/beat Factors determining “Stroke volume” are Preload Afterload Contractility

Stroke Volume Preload ~ the degree of ventricular filling during diastole Afterload ~ the pressure against which the ventricles must pump to eject blood during systole Contractility ~ myocardial contractile state

Preload Refers to the amount of stretch in the myocardial fibers at the end of diastole )just before the onset of systole) Usually this is thought of as the volume of blood in the ventricle at the end of diastole so is defined as the effective filling (or end-diastole) pressure of the ventricle The increase in pressure generated is related to the volume of blood in the ventricle and thus to the length of ventricular muscle fibers, the term preload is used clinically as an index of ventricular volume.

Preload Term preload is used interchangeably to reflect left ventricular filling pressures or venous return to the heart Any increase in venous return to the heart (e.g. increase in vent filling pressure) automatically forces an increase in CO by increasing SV The force of myocardial contraction is the function of its initial muscle fiber length The more these fibers are stretched, the more forcefully they contract, within physiologic limits. If stretched excessively, these muscle fibers develop less tension, resulting in decrease contractility

Preload Preload, then, is the function of the volume of blood presented to the left vent and the compliance (the ability of the vent to stretch) of the vent at the end of diastole This relationship is expressed as Starling’s Law ~ the greater the stretch the more forceful the contraction, but only up to a certain point Factors affecting volume include venous return, total blood volume, and atrial kick Factors affecting compliance are the stiffness and thickness of the muscle wall

Preload Ventricular – end diastolic pressures (or preload) are not measured directly, but indirectly Preload of the right ventricle is estimated by measuring central venous pressure (CVP) or right atrial pressure (RAP) Preload of the left ventricle is estimated by measuring left atrial pressure (LAP) or pulmonary capillary wedge pressure (PCWP, PAWP) Preload is best measured hemodynamically as the pulmonary artery wedge pressure or central venous pressure

Assessment of Preload Preload of the right ventricle is assessed by looking at the systemic venous system: Increased Right Heart Preload: Jugukar venous distention (JVD) Ascites Hepatic engorgement Peripheral edema Decreased right heart preload: Poor skin tugor Dry mucous membranes Orthostatic hypotension Flat jugular veins

Assessment of Preload Preload of the left ventricle is assessed by looking at the pulmonary venous system: Increased Left heart preload Dyspnea Cough Third heart sound (S3) Fourth heart sound (S4) S4 is the sound heard as blood bounces off stiff, noncompliant ventricular walls thus, indicating decreased contractility Decreased left heart preload There are no noninvasive assessments that indicate specifically diminished left ventricular preload. Usually, if the left heart has insufficient preload, the right heart has the same situation, and we can rely on signs of diminished right ventricular preload. In some cases S1 and S2 may be muffled

Factors affecting Preload Preload is affected by several factors. The arrows indicate the effect on preload: Heart rate Bradycardia ↑ Tachycardia ↓ Tricuspid/mitral valve disease Insufficiency ↑ Stenosis ↓ Volume of circulating fluid/blood Hypervolemia ↑ Hypovolemia ↓

Factors affecting Preload Drugs affecting venous tone Vasoconstrictors ↑ Vasodilators ↓ Intrathoracic pressure Spontaneous breathing ↑ Positive pressure ventilation ↓ Positive end-expiratory pressure (PEEP) ↓ Atrial systole Present ↑ Absent ↓

Afterload Defined as the resistance, or impedance, to ventricular ejection during systole There is an optimal amount of resistance necessary for the system to work properly Excessive afterload increases the workload of the heart, and increases the myocardial oxygen demand Afterload is largely determined by systemic vascular resistance (aortic end-diastolic pressure) and peripheral vascular resistance

Afterload In the clinical setting, afterload is not measured directly but is calculated (Calculation chart is provided at the end of lecture) Afterload of the right ventricle is primarily due to pulmonary vascular resistance (PVR) Normal PVR is 100 – 250 dynes/sec/cm -5 Afterload of the left ventricle is primarily due to systemic vascular resistance (SVR) Normal SVR is 800 – 1450 dynes/sec/cm -5 With smaller afterload (i.e. low SVR), the heart is able to contract more rapidly With a large afterload (i.e. high SVR), contraction is much slower

Factors affecting Afterload Afterload is affected by several factors. The arrows indicate the effect on afterload: Pulmonic/aortic valve disease Stenosis ↑ Insufficiency ↓ Arteriolar tone Vasoconstriction ↑ Vasodilation ↓ Viscosity of blood Polycythemia ↑ Anemia ↓ Drugs affecting arteriolar tone Vasoconstrictors ↑ Vasodilators ↓

Manipulation SVR (left heart) Decrease SVR by: IV NTG IV Niapride IV Hydralazine ACE inhibitors po Increase SVR by: IV Dopamine IV Dobutamine IV norepinephrine

Manipulation PVR (right heart) Increase PVR by: PEEP > 10 Mechanical ventilation Decrease PVR by: Low dose NTG IV Prostaglandin E (vasodilator, hormone secreted by kidney)

Contractility Refers to the intrinsic capacity of myocardial muscle fibers to shorten and/or develop tension In other words the ability of the myocardium to contract Clinically, there is no single measurement that defines contractility Rather, it can be inferred through clinical assessment and trends established via hemodynamic monitoring Increased contractility is referred to as a positive inotropism, a decrease as negative inotropism

Pulse Pressure The pulse pressure is the difference between diastolic and systolic blood pressure, normal being approximately 40 mm Hg The pulse pressure reflects how much the heart is able to raise the pressure in the arterial system with each beat Pulse pressure will increase when SV increases and/or arteriole vasoconstriction Pulse pressure drops with decreased SV and/or arteriole vasodilation ( ie. septic shock) Pulse pressure can be a useful, objective, and noninvasive indicator of myocardial contractility

Factors affecting Contractility Autonomic nervous system Sympathetic ↑ Parasympathetic ↓ Inotropic agents Positive inotropes ↑ Negative inotropes ↓ Electrolyte imbalance Hypercalcemia ↑ Hyperkalemia, hyponatremia ↓ Others LV preload Afterload myocardial oxygenation myocardial dysfunction

Manipulation of Cardiac Output

Pressure, Flow, and Resistance Understanding the relationship among pressure, flow and resistance can help you understand how cardiac output and vascular resistance relate to blood pressure These are relationships that are often manipulated in the acutely ill patient The relationship among flow, resistance and pressure can be mathematically expressed Flow x Resistance = Pressure

Pressure, Flow, and Resistance Flow and resistance can be adjusted to keep pressure steady The flow in the cardiovascular system is the CO, the resistance is the afterload and the pressure is the blood pressure

Normal Pressures When a catheter is passed through the venous system into the heart and pulmonary artery, certain pressure readings and wave forms are measurable During each individual section to follow, we will be looking at normal waveforms displayed depending on type of hemodynamic monitoring being used eg. arterial waveforms, CVP waveforms and PA waveforms To end this section I will leave you with the normal values. We will revisit them again during the sections to follow

Hemodynamic Pressures Central Venous Pressure (CVP) 0 – 6 mm Hg Right Arterial Pressures (RAP) Right Ventricular Pressures (RVP) Systolic 20 – 30 mm Hg Diastolic 2 – 8 mm Hg RV End Diastolic 2 – 6 mm Hg Pulmonary Artery Pressures (PAP) End diastolic 8 – 15 mm Hg Pulmonary Artery Wedge Pressures (PAWP) ~ (PAOP) ~ (PCWP) = 5 – 12 mm Hg

Hemodynamic Monitoring The high acuity patient has complex nursing needs The nurse requires a working knowledge of the determinants of cardiac output, preload, afterload, and contractility These determinants of cardiac output will be linked to the data available through hemodynamic monitoring with a pulmonary artery line This knowledge, coupled with astute observation and sharp assessment skills, can guide critical thinking at the bedside and provide a higher level of nursing care for the high acuity patient