Understanding Hemodynamics: Key Concepts and Clinical Relevance

Hemodynamics FALL SEMESTER 2023 Richard, Blackwell Hemodynamics - represents the governing principles of blood and its behavior in the blood vessels. ● Cardiac Output Review ○ CO= HRxSV ○ Stroke Volume is influenced by contractility, preload, and afterload ○ Contractility : the force of contraction reached by the ventricles. (PUMP) ○ Preload : degree of muscle fiber stretch before contraction (measurement of the volume in the ventricle prior to contraction) ■ If the heart has no filling time, will you have a decent preload? No. ○ Afterload : the amount of resistance the ventricle must push against during contraction. ■ How are the smooth muscles in your vascular system doing? Are they super tight (lots of resistance) or are they loose (no resistance at all)? 1

Hormone - Renin Angiotensin Contractility - how flexible (stretching) are your heart muscles, have you had a mi and muscle fiber has been replaced with scar tissue and that will decrease the amount of contractility. Heart rate faster will influence cardiac output the same as if it is slower. Inotrope - digoxin, cardiac glycosides and dobutamine. Catecholamines can increase the strength in contractions and degree of muscle stretch. Notice - the pressure inside the RA is pretty low. Blood is flowing into the RA passively from IVC/SVC. Pushed into the right ventricle. RV Muscle is thicker in the ventricle, so the pressure is higher during systole and relaxed during diastole. Then pushed into the pulmonary artery and pulmonary artery pressure is about the same as the right ventricle. When blood comes back to the lung, Left atrial side is higher than the right atrial side resistance. As the blood is flowing through, it’s exposed to higher and higher pressure. Right side has a lot less pressure than the left. Left side is stronger because it has to overcome systemic vascular pressure. Right side has to overcome pulmonary resistance. ● What is Hemodynamics? ■ Hemodynamics represents the governing principles of blood flow and its behavior in the blood vessels. - how the blood moves (behavior) in your body. ○ Can you get an idea of hemodynamic stability/instability without the invasive monitoring? ■ How? What Parameters could you examine ● Vital signs ○ Blood pressure is part volume, part resistance 2

● Inspect chest/NECK ● Auscultate heart & lungs ● Capillary refill ● Inspect Skin ● Monitor urine output ● Mental Status We can also look at cap refill (peripheral perfusion), organ perfusion will let us know whether we are hemodynamically stable or not. Assessment findings on patients will tell you a lot, monitors will help us but we can take care of a patient without it. ● Monitoring the pressures that determine contractility, volume, and resistance as the heart circulates blood throughout the body ○ Hemodynamic monitoring can separate resistance and volume. Blood pressure gives us it together. ● Who needs it? ○ Hemodynamic instability (shock, surgery, trauma) ○ Cardiac patients, cardiac surgery, Massive heart attack, surgery and the ICU. People we can look at and determine who is unstable. Blood pressure sucks, cap refill is no good. We should be able to tell. You won’t see this monitoring on a med surg floor but we would see in ICU/Surgery. ● What does it tell you? ○ Cardiac output and the factors that affect CO ○ Separate number for preload, afterload, left side and right side preload. Separate left side resistance and left side resistance. Breaking it all the way down. ○ Oxygen delivery and consumption ○ How well are our tissues receiving oxygen? If someone is really sick it will help to know where the specific problem is. Then we can fix it. 3

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● Non-invasive Blood Pressure (NIBP) gives a mixed picture of volume and resistance. With invasive monitoring, we can separate volume and resistance components. ○ We can really see all the pieces of it. ● Contractility ○ Too much (strong pump ) ■ Drugs ■ We normally don’t see contractility is too strong, maybe with cocaine. Most of the time if there is a pump problem it would be pump failure. ○ Too little ( pump failure) ■ Chronic heart failure ■ Myocardial Infarction ● Normally this is happening in a patient, weak heart. ● Pre-load could be too much (fluid overload, pump has failed causing a back up of fluid, you have a vasoconstrictive, vascular tone that is too much for pump to overcome, causing a backup..) Chronic HTN, backup will affect the lungs ● Preload ○ Too much (high volume ) ■ Fluid overload ■ Pump failure causing backup of blood & fluid ■ Vasoconstriction causing backup of blood & fluid ● Vascular resistance too high ● Chronic HTN, back up will affect the lungs ○ Too little (low volume ) ■ Fluid deficit (dehydration) ■ Blood loss 4

● G.I. bleed, traumatic amputation or blunt trauma that ruptured one of their organs. ■ Vasodilation ● Has our patient lost fluid, vomiting diarrhea, or have they lost blood. Have they had a GI bleed or a traumatic amputation? Blunt trauma that ruptured one of their organs. What kind of volume do they need? ● Afterload ○ Too much (high resistance ) ■ Vasoconstriction ● Primary hypertension ● Low volume ● Drugs ● Compensatory Mechanism for Low CO ○ If your volume is low, resistance goes up to maintain cardiac output. Body is trying to keep organs perfused. ○ Too little (low resistance ) ■ Vasodilation ● Drugs (nitrates for heart and then they to an ED drug) blood pressure hit the floor. ● Hypercapnia ○ CO2 gets too high, causing vasodilation. ● Distributive shock (septic, anaphylactic, neurogenic) ○ Some sort of hormonal or chemical problem that is causing blood vessel tone to relax everywhere. If we lose vessel tone, then there is no resistance. Conditions other than left ventricular failure may result in decreased cardiac output after an ACS. In about a third of patients with inferior MIs, right ventricular infarction and failure develop. In this instance, the right ventricle fails independently of the left. Decreased cardiac output with a paradoxical pulse, clear lungs, and jugular venous distention occurs when the patient is in semi-Fowler position.The desired outcome of management is to improve right ventricular stroke volume by increasing right ventricular fiber 5

stretch or preload. To enhance right ventricular preload, give sufficient fluids to increase right atrial pressure to 20 mm Hg. In the critical care unit, monitor the pulmonary artery occlusion pressure (PAOP), and auscultate the lungs to assess for left-sided heart failure. If symptoms of this complication occur, notify the health care provider immediately. If medical therapy is not sufficient to support the right ventricle and reverse the shock state, a right percutaneous ventricular assist device may be needed. This is a temporary measure to support the failing heart while treating the cardiogenic shock with medical therapy. - from learning plan ● Hemodynamic Parameters ○ Cardiac Output: SVxHR ○ Cardiac Index: measured cardiac output adjusted for body size ○ Two monitoring methods: ■ Intermittent Thermodilution: Using the Thermistor on the PA catheter ■ Continuous Cardiac Output: Specialized catheter ○ Central Venous Pressure (CVP): right-sided preload ■ Pressure in RA, how much volume is coming into RA ○ Mean Pulmonary Artery Pressure (PAPm): mean pressure exerted on the pulmonary artery, represents left-sided preload ■ Going to the lungs it's coming back to the left side 6

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○ Pulmonary Artery Occlusion Pressure (PAOP): obtained when the balloon on the PAC is inflated to wedge the catheter from the PA into a small capillary. This measures the pressure in the pulmonary capillaries, reflecting left ventricular end-diastolic pressure (left-sided preload) ■ Measurement of left side preload, we are actually measuring pressure in pulmonary capillaries, rather than big pulmonary arteries. This is right before blood gets back to the left side. More accurate. ● Inflate the balloon with no more than 1.5 ml of air, for no longer than 8-20 seconds, noting the waveform changes. ○ Why is this important? ○ The measurement is also known as “pulmonary capillary wedge pressure” ○ Pulmonary Vascular Resistance (PVR): resistance the right ventricle must overcome to open the pulmonic valve and eject a volume of blood into pulmonary vasculature. ■ Represents right-sided afterload ● Catheter is doing a calculation for us and will give a number, right sided afterload, how much pressure does the right ventricle have to push against in the pulmonary system. ○ Systemic Vascular Resistance (SVR): resistance the left ventricle must overcome to open the aortic valve and eject a volume of blood into the systemic circulation ■ Represents left-sided afterload ● How much does the left ventricle have to push against, this is giving us a picture of right and left sided afterload. What is our resistance? ○ Mixed Venous Oxygen Saturation (SvO2): measured with specialized pulmonary artery catheter 7

■ Telling you how well are tissues being oxygenated and are they absorbing the oxygen. We don’t do this with NCLEX regional medical centers. Don’t need to know this number. ■ Provides an assessment of balance between oxygen supply and demand. ■ Higher values indicate increased O2 supply, decreased O2 demand, or the inability to extract oxygen from blood (commons in sepsis) ■ Lower values indicate decreased O2 supply from low hemoglobin, low CO, low SaO2, and/ or increased O@ consumption ○ Intra-arterial pressures (measured with an arterial line) ○ Mean arterial pressure: MAP=DBP*2+SBP/3 ○ Benefits of having an arterial line: ■ Provides continuous BP monitoring ■ Blood draws including ABG’s without needle stick ■ Titrating vasoactive medications ● Gives us in real time arterial pressure second by second. Think about patients that are on medications that we are titrating based on blood pressure. How quickly can we adjust the IV pump? Minute to minute. If they are on a blood pressure medication like vasopressors or vasodilator (continuous iv drip) we need to know how is that working? mc/kg/min. We need to know how it is doing with our blood pressure. They benefit these types of patients with those medications listed above. ● Nursing responsibility for PAC Insertion ○ Informed consent 8

■ Check the chart, if they are not informed, get the doctor back in there to re explain. ○ Set up equipment ○ Proper position of patient ■ Trendelenburg common - if they can tolerate it ■ Towel roll between shoulder blades ○ Inserted with balloon deflated, until they get to a certain spot , selected inflation to “float” catheter into PA ○ Waveform changes as catheter progresses ■ We need to hook up so when we are inserting, we can see the waveform patterns. ■ So they will know when to blow up the balloon ○ Check for proper “wedging” for PAOP ○ Chest x-ray - CONFIRMS ● Monitoring Equipment: PA Catheter When the balloon is inflated, blood flow will carry it until it gets stuck, when the balloon is deflated, the catheter will sink into the RV and float in the pulmonary artery until it's inflated again. Then it will snake up. 9

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No one will ask you about the different color ports. We change the dressing every week/Thursdays at the lake (all central lines). Don’t leave it inflated and know how to take care of a patient that has one. Change it every thursday to change dressings on these as well. When you do a dressing change it will be sterile, administering fluids or medications a bubble is not okay. Connectors - connected to monitoring cables, cables that have a transducer (they are zeroed at the phlebostatic axis). There can be a bracket for this and arterial lines and they all get zeroed to the phlebostatic axis. Cables that are hooked up, inject port where you can give medicine, then you have distal is for thermodilution, distal infusion port for fluids or medicines. Cardiac output measurement we are doing something and then waiting for a number. What we are doing is pushing room temp saline through the thermistor port, it is passing through lumen closest to the metal part, this measures temperature, measuring how much and how quickly that cold water is coming through. Check the book for this, it's quite confusing. 10

As pulmonary capillary is being placed we are monitiroing. We get a waveform and a number reading. As they are pushing it in, we are watching that monitor. We know where it is based on, Different areas have different waveforms, our job as the nurse is to watch the wave form and number as it’s being placed to know where it is. If they don't stop pushing when they get to the pulmonary artery, we gotta say hang on. Once it's inflated they keep feeding until the balloon gets stuck and then the waveform changes from purple to red. It's sensing because there are sensors all along on the tube. Blow up once it's in the pulmonary artery, once it wedges, we deflate it . If we need to get a wedge pressure (PAOP), we blow up the balloon, wait for it to wedge, get the number and then deflate the balloon. If you blow it up and disconnect, it will deflate the balloon. 11

● Nursing Responsibilities for Arterial Line ○ Allen test for radial insertion ■ Make sure they have collateral pressure ○ Informed consent ○ Set up equipment (high pressure flush system) ○ Maintain the site, flush system (pressure bag at 300 mmHG), assess circulation every hour ■ If the patient's radial artery is destroyed or blocked, will they lose their hand? How would you know? Make sure they have good collateral pressure. ■ Take their hand, get a radial pulse and occlude it, on the opposite side of that radial is the ulnar, we occlude the ulnar. Hold down both sides of your wrist. Wait until their hand gets real pale, we will keep holding the radial pulse as tight as we can and we will let go of the ulnar side. We will see what happened to their hands. We are looking to see if that ulnar artery provides enough circulation to the hand. If the hand is pink, then that patient will survive without a radial artery. Even if we mess up that artery, that hand will be okay. Before they put the arterial line in. If it's pale, we don’t want to put the arterial line in that hand. We would look at the other hand. ■ Make sure the pressure bag stays under pressure, if not blood will run into that IV bag. Checking circulation in the hand every hour - cap refill. 12

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■ Mid axillary line - fourth intercostal space - phlebostatic axis - zeroed - atmospheric pressure. ● ● Monitoring Equipment: Arterial Line 13

● Complications of Invasive Monitoring ○ Vascular complication ■ Thrombosis ■ Hematoma ○ Infection ○ Bleeding ■ Or clots ○ Pneumothorax or Hemothorax ■ Inserted into the chest (long needle), they can easily drop a lung. ○ Cardiac dysrhythmias ■ Disrupting the blood flow, especially if the heart is irritated. ○ Pericardial tamponade ■ Poke through a vessel and bleed into a pericardial sac. It bleeds really fast. You will know right away. ● Ensuring Accuracy 14

○ Positioning the patient ■ If there chest moves higher of if they move, we have to re zero ○ Leveling the air-fluid interface (zeroing stopcock) to the phlebostatic axis ○ Zeroing the transducer (turn the stopcock off to the patient, allow atmospheric pressure to be read, the readout changes to zero) - for arterial line and pulmonary catheter. 15

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Numbers that we need to know. Don’t need to know purple numbers or Cardiac index. But we need to know what they mean. PVR is at 500 - that is high, what does it mean? Too much resistance in the pulmonary vascular resistance - pulmonary HTN, pulmonary embolism SVR - 800 - too much resistance in systemic vascular resistance - vessels are too contracted, we need to relax vessels SVR 500- too low, no vascular tone, we need to do something to tighten them up CVP - is one, they don’t have enough volume, may be fluid, may be blood. CVP - too much volume - we need to get rid of volume. How would we do it? Ace inhibitors keep you from retaining fluid but it also helps from contracting those vessels more. If we have a pump failure problem we may need to adjust Afterload and preload. Treat the underlying problem first. If there is pump failure as the base of the problem, let's give inotropes. ● Medication: Inotropes ○ Dobutamine ○ Amrinone & Milrinone (Inocor and Primacor) ■ Increase CO by increasing contractility ■ SVR & PVR decrease due to vasodilation 16

■ Reduces myocardial O2 consumption ■ Decreased PAOP,CVP, MAP ○ Need to be able to recognize an inotrope when you see one. Would we give it to a patient with cocaine overdose? No. Massive MI? Yep. They will improve contractility. If we improve the pump, It will help with the other two problems. ● Medications: Vasopressors - add a little resistance, contricts ○ Norepinephrine (Levophed) ○ Epinephrine ○ Phenylephrine (Neo-synephrine) ○ Dopamine (intropin) inotropic & vasopressor ■ Effect is dose dependent ● 0.5-5 mcg renal perfusion (causes visceral vasodilation ○ Little bit of dopamine - improve renal perfusion ● 5-20 mcg cardiac effects (increases HR, BP, SVR) ○ Higher dose vasoconstricts everywhere ○ Increase workload & O2 demand ■ Don't give vasopressor for pump failure. ○ Increase SVR & BP & HR ○ Tissue necrosis if extravasated ■ If it leaks outside of the vessel ■ Central line for vasopressor, medication can be given with central line. ● Medications: Vasodilators (Nitrate) ○ Reduce systemic vascular resistance ○ Nitroglycerine (Trifil) ■ Comes in glass bottle , use special tubing for administration ● It will absorb into plastic so don’t use regular tubing. ○ Nitroprusside (Nipride) - comes in opaque bag to (protect) block it from light ■ Wean off b/c may cause rebound HTN ■ Toxicity may occur if given >72 hours ■ Light sensitive, must be covered ○ Decreases preload, SVR & BP ○ If SVR too high vasodilator 17

Common Examples of Drug Therapy: Commonly used intravenous vasodilators and Inotropes Drug Category Selected Nursing Implications Nitrates Nitroprusside Sodium This agent is a potent, rapidly reversible vasodilator acting on both peripheral venous and arterial musculature. • Monitor BP every 2-5 minutes when initiating therapy. • Monitor PAOP, SVR, BP, heart rate, urine output frequently. Titrate medication to obtain the desired effect. Protect from light because this medication is light sensitive. Administered in micrograms per kilograms per minute (mcg/kg/min). Higher doses are associated with thiocyanate or cyanide toxicity. • Monitor for metabolic acidosis, confusion, and hyperreflexia, which are symptoms of toxicity. Nitroglycerin This agent produces systemic vasodilation and dilates coronary arteries rapidly. • Monitor BP every 1-3 minutes when initiating therapy because BP may drop in 1 minute. • Monitor RAP, PAOP, SVR, BP, HR, and urine output frequently. • Assess for headache because this is a frequent side effect of initial therapy. • Tolerance to this agent can develop with continued administration. Milrinone Fenoldopam Assess BP and HR every 5 minutes because hypotension is a common adverse effect. 18

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• If systolic BP drops 30 mm Hg, stop infusion and call the health care provider. Monitor I&O and weight because this drug causes diuresis. Sympathomimetics Dopamine This agent is a dose-dependent activator of alpha, beta, and dopaminergic receptors. • Assess reason for use and expected result. • Observe HR, BP, PAOP, SVR, cardiac output, and urine output every 5 minutes to 1 hour. • Titrate dosage to maintain dose range and obtain the desired effect. • Infuse through the central line because extravasation can cause tissue necrosis and sloughing. • Monitor for ectopy and angina Dobutamine Observe patients continuously during administration because this agent is a very strong beta 1 -receptor activator and a moderately strong beta 2 -receptor activator. • Titrate the drug on the basis of adequate tissue perfusion: mentation, skin temperature, peripheral pulses, PAOP, cardiac output, SVR, and urine output. Monitor for atrial and ventricular ectopy because dysrhythmias are an adverse effect 19

Low cardiac output Causes - decrease contractility, low volume, low resistance, weak pump Contractility problem - MI, Heart attack Volume - blood loss, dehydration - give them volume. CM - skin turgor, dry mucous membranes. Not enough pressure, low resistance - Distributive shock or too much vasodilator. Nitrates and viagra. Clinical Manifestations - Fatigue, low bp, hypotensive, decreased urine, decreased organ perfusion and pale. Interventions (improving) - if it's a weak pump (inotropic)(dobutamine), are they urinating, stable blood pressure. 20

Compensatory mechanism - if the patient has no circulating volume. HR goes up and the vascular tone increases because the body is trying to perfuse those organs. So if the volume is low the body will try to compensate. It works for a little while but not for very long. If they have a low CVP because that is their underlying problem from losing blood or volume. What will their SVR be? It will be high but it's not our underlying problem. We need to be able to resolve the cause. If we fix SVR, but we didn’t fix it, it will get worse. What if the volume is too much? diuretics . Vessels will try to relax a little bit to try to keep pressure at normal level. If SVR is low, If we give a vasopressor it could make them have higher pressure. More resistance will make it sky high. Treat the underlying problem not the compensatory mechanism. If my problem is high SVR, I won't have an immediate volume compensatory response. Too much resistance (give a vasodilator). Patient is getting better with stable BP, and SVR comes down and organs are perfusing. 21

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Resistance will try to compensate for low volume and vice versa. We need to fix the underlying issue. Volume does not compensate for resistance. Relaxed, we need to strengthen them up a bit. Vasopressors will help. Volume is okay but the resistance is the problem. We need to give them some resistance. Epinephrine, Dopamine, Norepinephrine and phenylephrine. 22

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