Module #8: Inflammation II Unit #1: Advanced Hemodynamic Monitoring PDF

Critical Care Nursing Program Module #8: Inflammation II Unit #1: Advanced Hemodynamic Monitoring Introduction As discussed in inflammation I, when cells become irritated or inf...

Critical Care Nursing Program Module #8: Inflammation II Unit #1: Advanced Hemodynamic Monitoring Introduction As discussed in inflammation I, when cells become irritated or inflamed, they release substances, such as histamine, prostaglandins and leukotrienes which cause the blood vessels to dilate and bring more blood to the injured area. This dilation causes a decreased preload, which in turn decreases the patient’s cardiac output. In order to pump blood and perfuse tissues, the body requires adequate preload or volume. This first unit, advanced hemodynamic monitoring, builds upon the basic hemodynamic monitoring concepts in your pumping and perfusion course. Advanced hemodynamic monitoring, as stated in the introduction to this unit is evolving with science, technology and evidence in critical care practice. In basic hemodynamic monitoring, we introduced you to central venous pressure monitoring (CVP) which is still used in some intensive care units, despite mounting evidence that it not be used clinically to guide fluid management in patients (Marik & Cavallazzi, 2013). New recommendations are to use functional hemodynamic indicators to guide fluid therapy and optimize stroke volume (Barros et. al, 2016; Johnson & Aherns, 2015). This unit will review guiding principles of hemodynamic monitoring, including usage of CVPs and pulmonary artery catheters. Pulmonary artery catheter (PA catheter, or sometimes called a Swan-Ganz catheter) usage is diminishing in clinical practice, as it is not associated with improved outcomes in many patient populations (Barros et. al, 2016). Pulmonary artery catheters are used to measure pulmonary artery pressures and provide information on patients volume status (preload), vascular resistance (afterload) and heart pumping ability (contractility). Collectively, these numbers combine to make a hemodynamic profile that reflects a patient’s condition. Newer, less, non-invasive and minimally invasive methods of optimizing stroke volume (determine if the patient is fluid responsive or non-responsive) to improve cardiac output are becoming more common in clinical practice and they will be explored. Shock and Acute Kidney Injury/Renal Failure will be discussed in further units as exemplars of inflammation. Learning Outcomes On completion of this unit, the learner will be able to: 1. Apply guiding principles when considering advanced hemodynamic monitoring. 2. Analyse the numerical values associated with pulmonary artery catheters. 3. Relate the appropriate interventions to correct hemodynamic instability when using advanced hemodynamic monitoring. 4. Discuss how passive leg raising can predict fluid responsiveness in critical care patients. 5. Explore less invasive hemodynamic monitoring methods. Module #8: Inflammation II Unit #1: Advanced Hemodynamic Monitoring Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 1 of 8  Critical Care Nursing Program Required Reading Please refer to your reading list for Inflammation II Guiding Principles for Advanced Hemodynamic Monitoring One of the first things to consider before using advanced hemodynamic monitoring is: Will this provide additional information to guide therapy? Is the therapy contraindicated or will the information provided outweigh the potential complication risks? (heart block, valve disease, embolism, PA rupture, PA infarct etc.) Can I obtain similar information using a non-invasive or minimally invasive method? Similar to basic hemodynamic monitoring, there are common principles when utilizing the information from advanced hemodynamic monitoring. 1. Single readings are not as significant as the trend of the pressure (e.g. is it increasing, decreasing, or staying stable). 2. Values must be interpreted in relation to the patient’s history, clinical course, interventions, and other parameters (e.g., mean arterial pressure). 3. To obtain accurate values, the transducer or water manometer must be levelled to the phlebostatic axis. Note: You are only responsible for memorizing the following parameters: CVP and CO. The normal ranges will be provided to you for the remaining parameters on examinations. However, you should understand what information each of the pulmonary artery values provide in relation to cardiac functioning. Thus, you are expected to interpret the patient’s pulmonary artery values on an exam but will be provided with the normal values. Central Venous Pressure (CVP)/Right Atrial Pressure (RAP) Recall from basic hemodynamic monitoring, that when learning to monitor and interpret hemodynamic monitoring and the related parameters, it is beneficial to start with a less complex parameter such as central venous pressure (CVP). Since CVP and right atrial pressure (RAP) are synonymous in that they both indicate the pressure in the right atrium, the term CVP will be used throughout this unit. Please refer to your reading list for Inflammation II Module #8: Inflammation II Unit #1: Advanced Hemodynamic Monitoring Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 2 of 8  Critical Care Nursing Program Normal CVP Value Normal CVP values vary from text to text. For purposes of this program, the normal CVP range used will be 2-6 mmHg. This value range is representative of a preload in a normal heart not a diseased patient. Therefore, it is common to see CVP readings that are higher clinically. Pulmonary Artery Pressures A PA catheter measures pulmonary artery pressures and, when the mitral valve is open, provides information about the pressure in the left ventricle at the end of diastole (LVEDP). This pressure is indicative of left ventricular function. Note: Since many areas do not use PA catheters, you are NOT responsible to know the setup of the system or perform an analysis of the waveforms. However, in your readings you will be shown the waveforms which will facilitate your understanding if you should work with a PA catheter in your future career. During insertion, the pressures in the right atrium, right ventricle and pulmonary artery are transmitted back to a cardiac monitor, which displays a unique waveform and pressure for each area. Please refer to your reading list for Inflammation II Positive pressure ventilation and the use of PEEP increase the pulmonary artery pressures. Therefore, it is important to be consistent in the manner in which the readings are obtained and watch the trends rather than individual numbers. Other Hemodynamic Parameters 1. Cardiac Output – Normal cardiac output is 4-8L/min. 2. Cardiac Index – CI is a very individualized number as it is based on A patient’s body surface area (e.g., height and weight are entered into monitors which then compute a CI). Normal cardiac index is 2.4-4L/minute. 3. The following example demonstrates the importance of calculating cardiac index. Patient A Patient B Height 183 cm (6’ 0”) 152 cm (5’ 0”) Weight 99 kg (218 lbs.) 55 kg (120 lbs.) BSA 2.22 m2 1.50 m2 CO 4.0 L/min 4.0 L/min CI 1.69 L/min/m2 3.4 L/min/m2 Module #8: Inflammation II Unit #1: Advanced Hemodynamic Monitoring Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 3 of 8  Critical Care Nursing Program Both patients have a cardiac output of 4.0 L/min, which falls within the normal range, but the CI for Patient A is well below normal and may suggest a shock state. However, for Patient B, the CI is within normal limits suggesting that the CO of 4 L/min is meeting this patient’s body requirements. 4. Pulmonary Vascular Resistance (PVR) – The amount of resistance that the right ventricle must overcome during systole. It will be affected by diseases such as COPD, septic shock and/or pulmonary embolus. Normal PVR is 100-250 dynes/sec/cm. 5. Systemic Vascular Resistance (SVR) – A measurement of left ventricular afterload. A very high SVR would indicate vasoconstriction whereas a very low SVR would indicate vasodilation. Normal SVR is 800-1400 dynes/sec/cm. 6. Mixed Venous Oxygen Saturation (SVO2) – A measurement of the bodies’ ability to provide an adequate supply of oxygen to meet the demand of the tissues. Normal SVO2 = 60%-80%. Module #8: Inflammation II Unit #1: Advanced Hemodynamic Monitoring Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 4 of 8  Critical Care Nursing Program You might find this table valuable when working with PA catheters. Less Invasive Hemodynamic Monitoring As reviewed in the introduction, PA catheters are not being used as frequently as in the past, as they have not been shown to improve patient outcomes. Research argues that CVP and PA catheters have limitations when used to determine the volume status of the patient and their fluid replacement needs (Johnson & Ahrens, 2015). Thus, other less or non-invasive methods of measuring pressures to reflect volumes are currently in use in other areas of the country, and being introduced in Nova Scotia (NS). The majority of these methods target stroke volume optimization, which works on the principle of a pulsus paradoxus and Frank Starling’s law of the heart (Ahrens, 2010). Techniques can range from passive leg raises (PLR) to finger-cuff to arterial pressure to transpulmonary thermodilution. Some methods require an accurate arterial line, some require both a femoral and thoracic central line. The goal is to optimize fluids, which Module #8: Inflammation II Unit #1: Advanced Hemodynamic Monitoring Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 5 of 8  Critical Care Nursing Program optimizes the patient’s preload, and thereby optimizes the patient’s stroke volume and subsequently the patient’s cardiac output. Other methods include bedside ultrasound examination of the vena cava, esophageal Doppler monitoring, CO₂ monitoring, and bioimpedance measurements. It is not the expectation that you understand how each of these individual devices (brands) work, but you should understand the basic principles underlying non-invasive and minimally invasive methods of hemodynamic monitoring. The table in your readings provides a great summary of these devices. Note: Doppler based hemodynamic monitoring methods and other hemodynamic monitoring devices (CO2 and bioimpedance) have not yet been adopted in NS. It is therefore not the expectation that learners memorize these forms of monitoring devices but rather understand what they may be used for. You will not be tested on these during examinations. Please refer to your reading list for Inflammation II Caring for Hemodynamically Unstable Patients So how do we apply advanced hemodynamic monitoring to our patients? How do we relate the information we gather from monitoring the patient to optimize pumping, perfusion and thus oxygenation of the tissues? Volume (or preload) is important to maintain cardiac output. Examine your patient and think - are the filling pressures (preload) adequate? Do they have a history which would lead you to believe they have a fluid volume deficit/overload? Is the HR too slow? (may cause decreased cardiac output if stroke volume cannot compensate). Is the HR too fast? (recall from pumping and perfusion that this may shorten diastole (filling time) and cause further myocardial ischemia). Is the afterload reduced? Does the patient look warm and vasodilated? Or is the afterload increased – does the patient feel cool peripherally/diminished pulses? The following chart should assist you when selecting treatment: Module #8: Inflammation II Unit #1: Advanced Hemodynamic Monitoring Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 6 of 8  Critical Care Nursing Program ADVANCED HEMODYNAMIC POTENTIAL TREATMENT/NURSING MONITORING PARAMETER CAUSES CONSIDERATIONS Decreased Right Ventricular Fluid volume Volume expanders- Preload deficit usually crystalloids (↓RAP/CVP) Vasodilation before colloids Vasoconstrictors once volume is replaced Increased Right Ventricular Fluid volume Diuretics Preload(↑RAP/CVP) overload Reduce intake Inability of RV to PCI/inotropic therapy pump fluid (ie. Like with an inferior AMI) Decreased Left Ventricular Fluid volume Volume expanders-usually Preload deficit crystalloids before colloids (↓PAWP or est. Using ↓PAD) Vasodilation Vasoconstrictors once volume is replaced Increased Left Ventricular Fluid volume Diuretics Preload overload Reduce intake (↑PAWP or estimate Using Inability of LV to Improve Contractility (PCI, or ↑PAD) pump fluid inotropic therapy) ↑Right Ventricular Afterload Pulmonary Pulmonary Vasodilators (↑PVR) Hypertension (oxygen, nitrous oxide, phosphodiesterase inhibitors like Sildenafil/Viagra) ↑Left Ventricular Afterload Chronic Vasodilators (↑SVR) hypertension (Nitroglycerin/Glycerol SNS trinidate) compensation ACE inhibitors ARBs ↓Left Ventricular Afterload Vasodilation Peripheral Vasoconstrictors (α (↓SVR) agents like Norepinephrine/Levophed, DOPamine/Intropine, Vasopressin/Antidiuretic hormone or Phenylephrine/Neosynephrine Decreased preload, increased Hypovolemia (fluid Replace fluids SVR (from compensation) volume deficit) Decreased SVR + Decreased Massive Fluids and vasoconstrictors + Preload Inflammatory treat infection response Increased Preload + Increased SNS compensation Diuretics and vasodilators SVR for decreased CO (Furosemide/Lasix and Nitroglycerin/Glycerol trinidate) Module #8: Inflammation II Unit #1: Advanced Hemodynamic Monitoring Copyright © 2022 Nova Scotia Health Learning Institute for Health Care Providers. All rights reserved Revised July 2022 Page 7 of 8  Critical Care Nursing Program ADVANCED HEMODYNAMIC POTENTIAL TREATMENT/NURSING MONITORING PARAMETER CAUSES CONSIDERATIONS Decreased cardiac ACS Oxygen to improve output/index (↓contractility) myocardial ischemia if sats