Welcome to the module on Determinants of Cardiac Output. This presentation was prepared for the critical care fellowship of the Inova health system.
The human heart is a pretty amazing organ. It is responsible for circulating all your blood volume every second of every minute of every day. Even when you are fast asleep your heart is working for you and luckily we don’t even have to think about it. The adult heart pumps about 5 quarts of blood each minute - approximately 2,000 gallons of blood each day - throughout the body. That’s a lot of blood! In one day the heart beats an average of about 100,000 times. In a 70-year lifetime, the average human heart beats more than 2.5 billion times. The Average weight of an adult heart can be from 9-12 oz. Some diseased hearts can weigh up to 2 lbs. Here is another interesting fact about your circulatory system. The network of blood vessels in your - arteries, veins and capillaries - is over 60,000 miles long. That's long enough to go around the world more than twice!
Lets discuss once again the basic anatomy of the heart. The right atria is a thin walled chamber that receives deoxygenated blood from the body. From the right atria, Blood then passes into the right ventricle past the tricuspid valve where it is then sent to the lungs via the pulmonary artery. It is important to recognize how Diseases of the lung can affect the way the heart muscle functions. For example if someone has COPD, PE, or mitral stenosis this causes increased resistance in the lungs. In turn, the heart has to pump harder to push past the area of resistance. Over time, this may cause right atrial enlargement or right atrial hypertrophy. Once the blood becomes oxygenated by the lungs it enters the left atrium via the pulmonary veins. Blood then enters the left ventricle through the mitral valve. Hemodynamics and blood flow within the heart can easily be affected by abnormalities of the valves or structures of the heart. Once in the left ventricle, which is a large thick walled chamber , the oxygenated blood is then pumped out to the rest of the body past the aortic valve and through the aorta. Left Ventricular Hypertrophy is the enlargement of the left ventricle. LVH can develop in response to high blood pressure, aortic valve stenosis, or an increased workload on the heart. In Aortic stenosis, the heart has to pump harder to overcome the resistance in the peripheral circulation. An understanding of the blood flow throughout the heart will help you to understand principles in hemodynamics.
This slide is a reflection of what is happening within the heart during different phases of the cardiac cycle. Diastole represents the ventricular relaxation phase in which the ventricles become filled with blood. During this phase the Tricuspid and Mitral valves are open and the atria empty blood into the ventricles. Valves open and close in response to pressure changes within the atria and ventricles. The coronary arteries fill during diastole. Systole represents the ventricular contraction and ejection phase in which blood is pushed out from the ventricles out to the rest of the body or to the lungs. During this phase the Pulmonic and Aortic valves are open. Blood is then rapidly ejected from ventricle into aorta or pulmonary artery.
The main goal of the hear tis to supply blood oxygen and other nutrients out to organs and body tissues. If our heart is not pumping effectively we will not have adequate perfusion to our vital organs.
Let’s first define hemodynamics. Hemodynamics is the Study of the movement and forces of blood within the cardiovascular system including the chambers & great vessels. Hemodynamics is Often monitored via the use of invasive lines and accompanying equipment but Can be obtained using direct and indirect measures
Why is it important for you to understand hemodynamics? Monitoring Hemodynamics Allows you to continually detect subtle changes in your patient. They can help you determine if there is a volume issue or pump issue. Allows the nurse to evaluate effectiveness of cardiac function such as cardiac output and perfusion to vital organs. Allows nurse to ensure that tissue oxygenation is adequate.
Understanding HD Allows the nurse to evaluate effectiveness of cardiac function. Allows nurse to ensure that cardiac output is enough to sustain perfusion to vital organs and that tissue oxygenation is adequate. If blood flow parameters are abnormal, you must consider it a threat to tissue oxygenation and consider interventions to improve cardiac function.
Indications for Hemodynamic monitoring include : Decreased cardiac output Hypovolemia Hemorrhage GI bleed Burns Shock (Cardiogenic, Septic, Neurogenic) Post Surgery Acute MI Cardiomyopathy Congestive Heart Failure All of these These conditions can affect tissue oxygenation and perfusion to vital organs.
Hemodynamic assessment can be obtained in multiple ways. The first parameter we will discuss is HR. The Best method for obtaining HR is an apical pulse. The apical pulse can be best heard at the Point of maximum impulse for 1 full minute. The PMI is located at the 5 th ICS midclavicular line. Measuring the apical pulse is more accurate than measuring the radial pulse (on average by 10 beats/minute). Measuring the pulse for 60 seconds is slightly more accurate than counting for 15 or 30 seconds, but only by 2 beats/minute. Sometimes it is helpful to Compare apical and peripheral pulses to ensure perfusion of beats.
Blood pressure monitoring is the most common indirect method for evaluating a patients hemodynamics at the bedside. Palpated BP is done with cuff and fingers over the artery while releasing cuff pressure and ausculating for heart sounds. Blood Pressure can also be doppled with the use of a doppler when heart sounds are difficult to auscultate. The use of a manual BP measurement is indicated for instances in which the BP machine is not picking up a BP reading. It helps to have both manual cuffs and Dinamaps machines available on the uint. PAWP-Pulm artery wedge pressure CO-cardiac output CI- cardiac index PVR- Pulmonic Vascular Resistance SVR-Systemic Vascular Resistance
Invasive arterial lines are more valid and reliable, and provide continuous blood pressure monitoring. Involves the use of transducer and amplifier and catheters placed in chamber in which the measurement is to be measured. Are connected to a flush system with a pressure bag set to flush at 3-5 mL/hr.
Pulmonary Artery Catheter (PA) is an invasive diagnostic catheter inserted into the pulmonary artery. It can provide us with lots of information about the pressures within the heart. Also knows as a Swan-Ganz catheter. The PA catheter can give us PAWP Pulmonary artery wedge pressure whichis the measure of the filling pressure in the left atrium. It can also provide measurement of CO, CVP, EF, and CI
Even without specialized equipment, a thorough Patient assessment will also give you clues about your patients hemodynamic state. Signs of inadequate perfusion include Cold Clammy skin, Pallor, cyanosis, Lightheadedness, Mental status changes, confusion or sudden lethargy Weak diminished pulses in the extremities are also sings of decreased circulation. Decreasesd urinary output and could dyspnea also signify poor perfusion
There are several factors that can influence cardiac function. These factors include the Autonomic Nervous System The Renin-Angiotensin System Electrolytes and other Diseases and or abnormalities of the circulatory system
The Autonomic Nervous System is an Internal regulating system that maintains homeostasis within the body. It is Composed of a network of nerves that send signals to the heart and other organs. Divided into Parasympathetic and Sympathetic systems the ANS plays a vital role in the control of blood pressure and heart rate regulation. Blood pressure is, at least on a moment-to-moment basis, regulated by a system for which the sensors are stretch-sensitive cells located in the neck arteries that carry blood from heart to brain. These sensors are known as baroreceptors An increase in blood pressure triggers sensor activity; their signal passes to the brain; and, in turn, the nerve supplying the heart (the vagus) is stimulated to release a chemicals (acetylcholine) that causes the heart to beat more slowly—which decreases blood pressure. The volume of the blood is subject to similar regulation. Fluid (mainly plasma) moves between the capillaries and the intercellular fluid in response to changes in pressure in the capillaries. A decrease in blood volume is detected by sensors at the base of the brain; the brain stimulates secretion of substances that cause contraction of tiny muscles surrounding the blood vessels that lead into the capillaries. The resulting arteriolar constriction reduces the flow of blood to, and the pressure within, the capillaries, so fluid moves from intercellular space into capillaries, thus restoring overall blood volume. This is achieved only if hemodynamic function is adequate. The body will always attempt to compensate when there is an imbalance within the Cardiovascular system. When there is a drop in BP the HR will increase to compensate. Why do you have to pee when it gets cold outside? When you get cold, the blood vessels in your extremities constrict so as to preserve blood flow to the vital organs. This life saving function explains why people survive severe cold even though their fingers, toes, nose and ears have frozen and fallen off. Before things get that bad, this shunting of blood from the periphery to the core essentially increases blood flow to the baroreceptors. In return the baroreceptors sense en excess fluid volume and send signals to the body telling it to diurese. This in turn increases urine production. Cold diureses is a real problem for parents of young children who want to play outside in the winter. You get them all bundled up in 12 layers, push them out the door and 10 minutes later they are back at the door crying that they have to pee, and you have to take off all 12 layers before they pee on themselves. The same thing happens with adults, so make sure you pee before you put on your winter clothes to go outside.
Baroreceptors respond very quickly to maintain a stable blood pressure, but they only respond to short term changes. Over a period of days or weeks they will reset to a new value. Thus, in people with essential hypertension the baroreceptors behave as if the elevated blood pressure is normal and aim to maintain this high blood pressure.
Consider your sympathetic response as the &quot;fight or flight“ response while and parasympathetic system stimulates the &quot;rest and digest“ response. When the parasympathetic nervous system is stimulated there is a release of Acetylcholine which slows closure of K channels, which leads to hyperpolarization of the cells, slowing activity of the SA and the AV node. The PS NS has little effect on the ventricles. When faced with an immediate threat, the Sympathetic nervous system is activated causing a release of epinepherine. This epinephrine Also speeds up the activity of the bundles of his and the purkinje fibers of the ventricles.which ultimately increases heart rate and strength of contractions.
The RAS plays an important role in maintaining blood volume and blood pressure. When blood pressure is low, the kidneys secrete a substance called renin . Renin stimulates the production of angiotensin . Angiotensin causes blood vessels to constrict resulting in increased blood pressure. Angiotensin also stimulates the secretion of the hormone aldosterone from the adrenal cortex . Aldosterone causes the tubules of the kidneys to retain sodium and water. This increases the volume of fluid in the body, which also increases blood pressure. If the renin-angiotensin-aldosterone system is too active, blood pressure will be too high. Aldosterone stimulates more Na reabsorption in the distal tubule, and water gets reabsorbed along with the Na. The increased Na and water reabsorption from the distal tubule reduces urine output and increases the circulating blood volume. There are many drugs which interrupt different steps in this system to lower blood pressure. Use of These drugs can help control high blood pressure.
Beta1 receptors are located in the kidneys. Stimulation of β1 receptors on the kidney causes renin release. Beta blockers work by blocking this renin release thus resulting in decrease of Blood pressure. ACE inhibitors prevent the angiotensin converting enzyme (ACE) from producing angiotensin II . Angiotensin II is responsible for constriction of smooth muscle surrounding arterioles. So when this mechanism is inhibited, the result is a decreased blood pressure. Angiotensin receptor blockers (ARBS) block the activation of angiotensin II, causing vasodilation and ultimately a reduction in blood pressure. Aldosterone is a hormone that increases sodium and water reabsorptoin in the renal tubules. Spironolactone is a drug that blocks this response and thus promoting diuresis. Keep in mind that plasma levels of aldosterone increase progressively in heart failure. This phenomenon of aldosterone escape is associated with adverse outcome. The aldosterone receptor antagonists spironolactone and eplerenone can improve prognosis for patients with heart failure. The commonest, and often problematic unwanted effect of these agents, hyperkalaemia. Direct renin inhibitors block the enzyme renin from triggering a process that helps regulate blood pressure. The recent approval of aliskiren (Tekturna; Novartis)—the first drug in a new class of antihypertensives that inhibits the renin-angiotensin system (RAS) by directly targeting the renin enzyme—is also the first approval of a new class of antihypertensives in more than a decade.
Electrolyte levels play a vital role in the proper functioning of heart muscle. Potassium (K+) is most abundant intracellular ion and The concentration of potassium in the cells determines the excitability of the nerve and muscle cells. Significant changes can have life-threatening consequences. Peaked t-waves are indicative of hyperkalemia. Magnesium (Mg) is the second most common intracellular ion. Magnesium is Necessary for the movement of sodium, potassium and calcium across the cellular membrane, as well as stabilization of the cell membrane. Low magnesium in combination with low potassium is a risk factor for severe dysrhythmias. In heart muscle tissue, Ca2+ regulates muscle contraction. Electrical signals that determine the cardiac rhythm within the heart rely on an adequate supply of calcium. Most calcium channel blockers decrease the force of contraction of the myocardium (muscle of the heart). This is known as the negative inotropic effect of calcium channel blockers. It is because of the negative inotropic effects of most calcium channel blockers that they are avoided (or used with caution) in individuals with cardiomyopathy . Many calcium channel blockers also slow down the conduction of electrical activity within the heart, by blocking the calcium channel during the plateau phase of the action potential of the heart (see: cardiac action potential ). This results in a negative chronotropic effect resulting in a lowering of the heart rate and the potential for heart block . The negative chronotropic effects of calcium channel blockers make them a commonly used class of agents in individuals with atrial fibrillation or flutter in whom control of the heart rate is an issue.
There are some heart conditions that affect cardiac function and hemodynamics. cardiomyopathies are shows in this illustration. For comparison the normal architecture of the left ventrilce is shown in the top right illustration. In DCM the left ventricle shows increase in size and volume. In HCM the ventricular walls are thick and the ventricular chamber is consequently reduced in volume. In RCM the ventricular wall may or may not be thicker. The restriction to the wall movement may be due to disease(s) that affect the endocardium of the heart or that actually infiltrate the myocardium. Amyloid, an unusual protein not normally present in the body, may accumulate in heart muscle and other tissues, causing amyloidosis. In RCM the heart muscle is gradually replaced by scar tissue. Scarring may result from injury due to radiation therapy for cancer. In the other type, abnormal substances accumulate in or infiltrate the heart muscle resulting in reduced blood volume within the heart.
Here is a list of some other cardiac conditions that can affect hemodynamics. They include Atrial Fibrillation Aortic Stenosis Bradycardia Cardiac Tamponade Heart Blocks Myocardial Infarction Supraventricular Tachycardias Ventricular Arrhythmias
In order to get a grasp on Hemodynamics lets first review some of the basic terminology you will see used to describe cardiac function. In the following slides we will discuss each of these terms in detail.
Heart rate is Controlled by the Autonomic Nervous System As previously discussed the SA node is stimulated by sympathetic and parasympathetic innervations Sympathetic innervation via the Neurotransmitter: Epinepherine and Norepinepherine- speeds up heart rate Parasympathetic innervation via the Neurotransmitter: Acetylcholine – slows down heart rate During a state of low perfusion or low blood pressure, the body may compensate by increasing heart rate.
Conditions that increase HR include Fever Bleeding Hypovolemia Anxiety Excercise Excessive Caffeine or other stimulants Pain Keep in mind that during a state of low perfusion or low blood pressure, the body may compensate by increasing heart rate.
Medications can also speed up heart rate. Meds that increase Heart Rate include Atropine Epinepherine and Dopamine (2-10mcg/kg/min) Pacemaker is a device which can also increase heart rate and is considered if heart rate remains slow and patient symptomatic.
Certain Conditions can cause slow heart rate. These conditions include sleep, Old age or being very athletic, Hypothermia, Hypothyroidism, and Conduction disturbances known as heart blocks. Vagal stimulation from vomiting or bearing down will also slow heart rate.
Medications that decrease heart rate include Adenosine Beta Blockers (Atenolol, Metroprolol, Coreg) Digoxin Calcium Channel Blockers (Cardizem) Remember to avoid Cardizem with LV dysfunction due to negative inotropic effects.
Now that we have discussed heart rate, lets discuss cardiac output. CO is defined as the volume of blood being pumped by the heart , in particular by a ventricle in a minute. Right and left ventricle eject about the same amount of stroke volume with each beat. The simple formula used to obtain cardiac output is Heart rate times stroke volume. For example if your Heart Rate is 100bpm And your Stroke Volume is 50mL/beat CO=5,000 mL per min or 5 L/min Normal CO is 4-6 L/min
Low cardiac output can be can occur as a result of the ventricle not filling adequatelely. This occurs during Tachycardia Rhythm disturbances Hypovolemia Mitral or Tricuspid Stenosis Pulmonic Stenosis Constrictive Pericarditis or Tamponade and or Restrictive Cardiomyopathy
High cardiac output in a normal healthy diseased free individual occurs in response to stress, exercise, or anxiety. While in the hospital sudden high cardiac output can indicate an underlying problem. For example Sepsis causes a hyper dynamic state in which vasodilaton occurs and systemic vascular resistance to decreases. This decrease produces an initial compensatory increase in CO. Remember that CO elevation is a symptom of a problem. Treat what may be causing the problem and CO should return to normal.
Stroke volume is defined at the Volume of blood ejected from each ventricle with each heartbeat Normal stroke volume is approximately 50-100 mL per beat i. Stroke volume is dependant on Preload, afterload and contractility. We will discuss each of these components in more detail over the next few slides. Since CO is a product of SV x HR any change in the stroke volume will normally produce a change in the heart rate. If the SV is elevated, the HR may decrease. (eg. In adaptation to exercise). An exception to this guideline is during an increase in metabolic rate, where both the SV and HR increase. If the SV falls, the HR will normally increase. To increase cardiac output, attempt to increase stroke volume by decreasing heart rate.
Preload is the length to which a myocardial cell is stretched prior to the next contraction. The heart is a dynamic pump that will vary its output dependant on the amount of blood it receives. The degree to which a mycoardial cell is stretched determines the force during the contraction (systole). Note that the pressure, volume, and stretch are directly proportional to each other. The more volume in the heart, the greater the stretch resulting in a stronger contraction. Think of preload as volume and just like your gas tank in your car, ask yourself how full is the tank? If the tank isn’t full the heart is not going to pump.
Preload is Affected by Absolute blood volume (how much blood is in body) hemorrhage, fluid overload (iv fluids, heart failure, renal failure) Distriubtion of blood in body (where is the blood within the body) Atrial kick which delivers 20% of co to ventricles (ie afib) Ventricular function (typically decreased in Heart failure) Ventricular compliance (how distensible the ventricles are==if very stiff, do not expand properly, and so don’t fill properly, and so doesn’t eject properly)
Reasons in which a patient may have increased Preload include: Increased circulating volume/hypervolemia Mitral insufficiency Aortic insufficiency and Heart Failure Decreased Preload can be seen in Decreased circulating volume (bleeding, third spacing) Mitral stenosis Vasodilator use (NTG) Asynchrony of atria and ventricles Cardiac tamponade Atrial Fib
At times it may be necessary to improve your patients cardiac status and tissue perfusion. To Increase Preload consider Administering IV fluids (0.9% NS, LR), vasopressors(only effective if tank is “full”) such as Levophed, Dopamine, or Norepinepherine Administer Blood and or blood products Or consdider volume expanders such as Hetastarch or , albumin When your patient is fluid overloaded such as in cardiomyopathy or heart failure , you want to consider interventions to decrease preload such as Adminster diruetics Lasix or Aldactone It also may help to consider Vasodilators such as nitrates or morphine
Afterload is defined as the force against which the ventricle must eject blood during systole. The right ventricle must push against the resistance in the lungs while the left ventricle must overcome the Systemic Vascular Resistance. The SV is six times the pressure present in the pulmonary circuit.
Any forces that oppose ventricular ejection can contribute to Afterload. These include: ventricular outflow obstructions as seen in aortic stenosis, Sympathetic nervous system stimulation which causes vasoonstriction, hypertensive states, and Hypercoagulable states. Examples of hypercoagulable states include post-op patients, women taking estrogens or birth control pills, and some cancer patients.
Now that you have an understanding of afterload, lets discuss interventions used to increase it. When your goal is to shunt blood to core organs consider vasoconstrictors such as Dopamine, epnepherine, or norepinehperine. In low to moderate doses (less than 10 mcg/kg/minute), dopamine stimulates the dopaminergic receptor sites and produces renal, mesenteric, coronary, and intracerebral vasodilation. Dopamine effect is mild at low doses and effect increases as dose increases. The drug's positive inotropic and chronotropic effects also increase cardiac output. In contrast, doses over 10 mcg/kg/minute produce alpha-receptor stimulation and vasoconstriction of the peripheral and renal arteries which is used in severe cardiogenic shock. IMPORTANT NOTE: Renal shutdown may occur at doses greater than 50 micrograms/kilogram/minute. The infusion rate should be reduced if urine flow decreases without adequate peripheral effects. Administer into large vein to prevent the possibility of extravasation (central line administration). Typical renal dose is 3mcg/kg/min intravenous dobutamine , which acts on β1 receptors of the heart leading to increased contractility and heart rate As afterload increases, cardiac output decreases Remember that preload changes only secondarily to changes in afterload. In times of hypovolemic states be sure to correct the hypvolemia with volume before using the vasopressors or the vasopressors will be in effective.
Now lets discuss interventions to decease afterload. These include administration of vasodilators which decrease afterload by decreasing the resistance in the systemic circulation. Arterial Dilators that decrease afterload include Morphine, Nitroprusside, Hydralazine, Clonidine, Labetelol, Ace Inhibitors, ARBs. Intra aortic balloon pumps help decrease afterload. Intraaortic balloon pumps help by increasing coronary blood flow, improving myocardial oxygen supply, and contractility while decreasing afterload.
The last component that determines cardiac output is conractility. Contractility refers to the inherent ability of the myocardium to contract normally. Contractility is influenced by preload and is affected by: Ventricular muscle mass Heart Rate Oxygen status Chemical or pharm effects
There is no way to measure contracility of the heart directly, but we can assess contractile state of the heart indirectly by assessing cardiac output. Now lets discuss conditions that improve contractility of the heart muscle. Stimulation of the sympathetic nervous system will stimulate an increase in heart rate and contractility of the heart. Calcium is necessary for heart muscle to function properly and without it, cardiac contraction may not be as effective. effects of severe hypercalcemia can induce cardiac arrhythmias. Muscles, including the heart, do not receive appropriate impulse signals: This results in muscle weakness and heartbeat abnormalities. The use of positive inotropic drugs such as digitalis, milrinone, epinepherine, and dobutamine improve contractility. Medications that increases the strength of cardiac contraction will Increase EF, SV, Cardiac Output, and tissue oxygenation. Consider the use of Positive inotropic agents increase myocardial contractility, and support cardiac function in conditions such as decompensated congestive heart failure, cardiogenic shock, septic shock, myocardial infarction, cardiomyopathy, etc.
Drugs that decrease contractility of the heart are known as Negative inotropes an include Beta blockers, calcium channel blockers, and barbituates. Keep in mind that some antidysrhythmics can dec. contractility as well. Myocardial ischemia and or infarction will dec. contractility as well as CM vagal stimulation, hypoxemia, and metabolic acidotic states.
Now lets look at how it is all related. Cardiac output is determined by heart rate and stroke volume. Heart rate set by the SA node. The stroke volume depends on Preload, Afterload, and contractility of the heart.
Now lets discuss some other terms you will hear that are used to describe some of the hemodynamic aspects of your patient. Mean Arterial Pressure or MAP Constant and adequate pressure in the arterial system is required to drive blood into all of the organs. Abnormally low blood pressure results in inadequate perfusion of organs, while abnormally high blood pressure can cause heart disease, vascular disease and stroke. Therefore, it is essential that blood pressure be maintained within a narrow range of values that is consistent with the needs of the tissues. Mean arterial pressure represents the average pressure in the arterial system. This value is important because it is the difference between MAP and the venous pressure that drives blood through the capillaries of the organs. Because more time is spent in diastole than in systole, MAP is not simply the average of the systolic and diastolic pressures. A simple formula for calculation of MAP is 2 times the diastolic pressure plush the systolic pressure divided by 3. MAP obtained using formula are inaccurate if Pulse greater than 60 because the formula assumes that diastole comprises 2/3rds of the cardiac cycle. The Mean arterial pressure required to perfuse adequately may differ from patient to patient and will depend on other underlying cardiac diseases and goals of treatment.
Cardiac Index represents the expected cardiac output based on body surface area. The normal range for CI is 2.5-4.0 L/min/m2. If the CI falls below 1.8 L/min, the patient may be in shock.
The amount of blood estimated to be pumped out of the LV to the rest of the body with each heartbeat. Normal range is 50- 75%. Systolic dysfunction occurs when EF falls below 50%. Systolic dysfunction is the inability of the LV to effectively pump blood to the rest of the body. As SV decreases, the body compensates by retaining water and sodium, whick ultimately leads to an increase in SV and pulmonary congestion. Ejection fraction can be Measured by echocardiogram, nuclear study, MRI, CT.
Remember that you don’t just want to rely on machinery and equipment to tell you what is going on with your patient. To get a clearer clinical picture of your patients hemodynamic status look for the following assessment findings that could indicate compromised hemodynammics. These include. Drop in BP Rapid weak pulses Change in LOC Cold, mottled, cyanotic skin Tachycardia Tachypnea Complaints of lightheadedness Decreased urine output Hypoxia and or Edema
It is important to know patients baseline BP. If pt. baseline BP is normally pretty high, may not tolerate BPs that are lower (vital organs may not get perfused). Keep in mind that the higher a patients HR the more likely the heart will consume more oxygen. In patients with altered myocardial blood flow, keep HR low to protect myocardial function. To decrease workload of the heart consider grouping patient activities throughout the shift. BP generally will not drop until HR and SVR increases can no longer compensate. Drop in BP usually a late sign of a problem since compensatory mechanisms initially serve to keep BP normal. Use caution when lowering BP to rapidly. Pt’s who are used to ↑BPs can have a dec. in organ perfusion at higher pressures than you would expect. Remember that in In states of low perfusion or low BP, body compensates by increasing heart rate.
This concludes the module on Determinants of Cardiac Output.
Determinants of cardiac output for captivate
Determinants of Cardiac Output Intro to Tele Leslie Binder MSN, RN
Heart Facts <ul><li>The adult heart pumps about 5 quarts of blood each minute - approximately 2,000 gallons of blood each day - throughout the body. </li></ul><ul><li>The heart beats about 100,000 times each day. </li></ul><ul><li>In a 70-year lifetime, the average human heart beats more than 2.5 billion times. </li></ul>
Goal of the Heart <ul><li>Main goal of the heart is to get blood and oxygen to organs and body tissues. </li></ul>Blood Oxygen and Glucose
Hemodynamics <ul><ul><li>Study of the movement and forces of blood within the cardiovascular system (chambers & great vessels) </li></ul></ul><ul><ul><li>Often monitored via the use of invasive lines and accompanying equipment </li></ul></ul><ul><ul><li>Can be obtained using direct and indirect measures </li></ul></ul>
Why is understanding hemodynamics so important?
Hemodynamics will help you evaluate the effectiveness of your patients cardiac function.
Indications for Hemodynamic Monitoring <ul><li>Decreased cardiac output </li></ul><ul><li>Hypovolemia </li></ul><ul><li>Hemorrhage </li></ul><ul><li>GI bleed </li></ul><ul><li>Burns </li></ul><ul><li>Shock (Cardiogenic, Septic, Neurogenic) </li></ul><ul><li>Post Surgery </li></ul><ul><li>Acute MI </li></ul><ul><li>Cardiomyopathy </li></ul><ul><li>Congestive Heart Failure </li></ul>
Methods of Obtaining Hemodynamic Measurements Heart Rate
Factors Influencing Cardiac Function <ul><li>Autonomic Nervous System </li></ul><ul><li>Renin-Angiotensin System </li></ul><ul><li>Electrolytes </li></ul><ul><li>Diseases and or abnormalities of the circulatory system </li></ul>
Autonomic Nervous System <ul><li>Internal regulating system that maintains homeostasis within the body. </li></ul><ul><li>Composed of a network of nerves that send signals to the heart and other organs. </li></ul><ul><li>Divided into Parasympathetic and Sympathetic Nervous System. </li></ul><ul><li>Baroreceptors play a role in </li></ul><ul><li>blood pressure regulation. </li></ul>
Baroreceptors and Chronic Hypertension Do not drop BP too low too fast especially in those with chronic hypertension.
Cardiac Output <ul><li>CO= HR x SV </li></ul><ul><li>Example: </li></ul><ul><ul><li>Heart Rate 100bpm </li></ul></ul><ul><ul><li>Stroke Volume 50mL/beat </li></ul></ul><ul><ul><li>CO=5,000 mL per min or 5 L/min </li></ul></ul><ul><ul><li>Normal CO is 4-6 L/min </li></ul></ul>
Factors Causing Low Cardiac Output <ul><li>Inadequate Left Ventricular Filling </li></ul><ul><ul><li>Tachycardia </li></ul></ul><ul><ul><li>Rhythm disturbance </li></ul></ul><ul><ul><li>Hypovolemia </li></ul></ul><ul><ul><li>Mitral or Tricuspid Stenosis </li></ul></ul><ul><ul><li>Pulmonic Stenosis </li></ul></ul><ul><ul><li>Constrictive Pericarditis or Tamponade </li></ul></ul><ul><ul><li>Restrictive Cardiomyopathy </li></ul></ul>
Factors Causing Low Cardiac Output <ul><li>Inadequate Left Ventricular Ejection </li></ul><ul><ul><li>Coronary Artery Disease causing LV ischemia or infarction </li></ul></ul><ul><ul><li>Myocarditis or cardiomyopathy </li></ul></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Aortic Stenosis </li></ul></ul><ul><ul><li>Mitral Regurgitation </li></ul></ul><ul><ul><li>Drugs that are negative inotropes </li></ul></ul><ul><ul><li>Metabolic disorders </li></ul></ul>
High Cardiac Output <ul><li>Healthy patient </li></ul><ul><ul><li>CO ↑ secondary to increased 02 demand (exercise, fear, anxiety). </li></ul></ul><ul><li>In hospital </li></ul><ul><ul><li>Response to systemic inflammation (Sepsis). </li></ul></ul>
Stroke Volume <ul><li>Stroke Volume </li></ul><ul><ul><li>Volume of blood ejected from each ventricle with each heartbeat </li></ul></ul><ul><ul><li>Normal 50-100 mL per beat </li></ul></ul><ul><ul><li>Decreased SV= increased HR </li></ul></ul>Determinants of Stroke Volume Preload Afterload Contractility
Preload <ul><li>Stretch of the ventricular wall </li></ul><ul><li>Usually related to volume </li></ul><ul><li>Frank Starlings Law: </li></ul><ul><li>How full is the tank? </li></ul>
Preload <ul><li>Factors affecting preload: </li></ul><ul><ul><li>Absolute blood volume </li></ul></ul><ul><ul><li>Distribution of blood in body </li></ul></ul><ul><ul><li>Atrial kick </li></ul></ul><ul><ul><li>Ventricular function </li></ul></ul><ul><ul><li>Ventricular compliance </li></ul></ul>
Conditions Affecting Preload <ul><li>Increased Preload seen in: </li></ul><ul><ul><li>Increased circulating volume/hypervolemia </li></ul></ul><ul><ul><li>Mitral insufficiency </li></ul></ul><ul><ul><li>Aortic insufficiency </li></ul></ul><ul><ul><li>Heart Failure </li></ul></ul><ul><li>Decreased Preload seen in: </li></ul><ul><ul><li>Decreased circulating volume (bleeding, third spacing) </li></ul></ul><ul><ul><li>Mitral stenosis </li></ul></ul><ul><ul><li>Vasodilator use (NTG) </li></ul></ul><ul><ul><li>Asynchrony of atria and ventricles </li></ul></ul><ul><ul><li>Cardiac tamponade </li></ul></ul><ul><ul><li>Atrial Fib </li></ul></ul>
Interventions Affecting Preload <ul><li>To Increase Preload </li></ul><ul><ul><li>Fluids (0.9% NS, LR) </li></ul></ul><ul><ul><li>Vasopressors (only effective if tank is “full”) </li></ul></ul><ul><ul><li>Blood and or blood products </li></ul></ul><ul><ul><li>Volume expanders </li></ul></ul><ul><li>Decrease Preload </li></ul><ul><ul><li>Diuretics </li></ul></ul><ul><ul><ul><li>Lasix, Aldactone </li></ul></ul></ul><ul><ul><li>Vasodilators such as nitrates, Morphine </li></ul></ul>
Afterload <ul><li>The resistance or pressure which the ventricle must overcome to eject its volume of blood during contraction. </li></ul><ul><li>Right Ventricle </li></ul><ul><ul><li>Pulmonary Vascular Resistance (PVR) </li></ul></ul><ul><li>Left Ventricle </li></ul><ul><ul><li>Systemic Vascular Resistance (SVR) </li></ul></ul>
Contractility <ul><li>Refers to the inherent ability of the myocardium to contract normally. Contractility is influenced by preload. </li></ul><ul><li>Affected by: </li></ul><ul><ul><li>Ventricular muscle mass </li></ul></ul><ul><ul><li>Heart Rate </li></ul></ul><ul><ul><li>Oxygen status </li></ul></ul><ul><ul><li>Chemical or pharmacological effects </li></ul></ul>
Conditions That Increase Contractility <ul><li>Sympathetic Stimulation </li></ul><ul><ul><li>Fear or anxiety </li></ul></ul><ul><li>Calcium </li></ul><ul><li>Inotropes </li></ul><ul><ul><li>Digitalis </li></ul></ul><ul><ul><li>Milrinone </li></ul></ul><ul><ul><li>Epinepherine </li></ul></ul><ul><ul><li>Dobutamine </li></ul></ul>
Conditions That Decrease Contractility <ul><li>Negative Inotropes </li></ul><ul><ul><li>Beta Blockers, Calcium Channel Blockers, barbituates and most antidysrythmics. </li></ul></ul><ul><li>Infarction </li></ul><ul><li>Cardiomyopathy </li></ul><ul><li>Vagal Stimulation </li></ul><ul><li>Hypoxemia </li></ul><ul><li>Acidosis </li></ul>
How it’s all related Cardiac Output Heart Rate Stroke Volume Preload Afterload Contractility Usually set by SA node
Mean Arterial Pressure <ul><li>MAP is considered to be the perfusion pressure seen by the organs in the body. </li></ul><ul><li>Goal = MAP > 60mm/Hg </li></ul><ul><li><60 leads to ischemia </li></ul><ul><li>Calculated MAP= 2 x Dialstolic +Systolic </li></ul><ul><ul><ul><ul><ul><li>3 </li></ul></ul></ul></ul></ul>
Pulse Pressure <ul><li>Difference between systolic and diastolic pressures </li></ul><ul><ul><li>Representative of Stroke Volume and arterial capacitance </li></ul></ul><ul><ul><li>Normal range 30-40mm/Hg </li></ul></ul><ul><ul><li>Changes in pulse pressure can indicate certain conditions (exercise, shock, heart failure). </li></ul></ul>
Cardiac Index <ul><li>CI = CO/BSA </li></ul><ul><li>Normal range for CI is 2.5-4.0 L/min/m² </li></ul>
Ejection Fraction <ul><li>The amount of blood estimated to be pumped out of the LV to the rest of the body with each heartbeat. </li></ul><ul><li>Normal range is 50- 75%. </li></ul><ul><li>Systolic dysfunction occurs when EF falls below 50%. </li></ul><ul><li>Measured by echocardiogram, nuclear study, MRI, CT. </li></ul>
Assessment Findings in Compromised Hemodynamics <ul><li>Drop in BP </li></ul><ul><li>Rapid weak pulses </li></ul><ul><li>Change in LOC </li></ul><ul><li>Cold, mottled, cyanotic skin </li></ul><ul><li>Tachycardia </li></ul><ul><li>Tachypnea </li></ul><ul><li>Complaints of lightheadedness </li></ul><ul><li>Decreased urine output </li></ul><ul><li>Hypoxia </li></ul><ul><li>Edema </li></ul>
Nursing Considerations <ul><li>Know your patient’s baseline blood pressure. </li></ul><ul><li>Rapid heart rates lead to more oxygen consumed. </li></ul><ul><li>To decrease workload of the heart consider grouping patient activities throughout the shift. </li></ul><ul><li>Use caution when lowering blood pressure too rapidly in patients with chronic HTN. </li></ul><ul><li>In states of low perfusion or low BP, body compensates by increasing heart rate. </li></ul>