NTI 2010 Boot Camp. Paradigm Shift. Hemodynamics: Cardiac Output. Basic Hemodynamic Formula

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1 Cardiovascular Assessment and Hemodynamic Principles NTI 2010 Boot Camp Hemodynamics does not equal invasive monitoring Paradigm Shift Karen Marzlin MSN, RN, CCNS, CCRN-CMC Cardiovascular Nursing Education Associates Circulation: Heart Arteries Veins Blood Volume 3 4 Hemodynamics: Cardiac Output Understanding basic hemodynamic principles and their impact on the forward propulsion of blood. Basic Hemodynamic Formula Cardiac Output Heart Rate X Stroke Volume Preload Afterload Contractility Stroke Volume: Volume of blood ejected with each beat ml/beat 5 6 Associates 1

2 Cardiac Output Right Sided vs. Left Side System Volume of blood ejected by the ventricle each minute Measures effectiveness of the heart as a pump Other terms: Stroke Volume: Volume of blood ejected with each beat. Normal: ml/beat Ejection Fraction: Percent of blood ejected from the ventricle Normal: 55%-60% 7 8 Preload Right and Left Sided Preload End-diastolic stretch on myocardial muscles fibers Determined by: Volume of blood filling the ventricle at end of diastole Greater the volume the greater the stretch (muscle fiber length) Greater the stretch the greater the contraction Greater the contraction the greater cardiac output TO A POINT Right Preload Measured by right atrial pressure (RAP) or central venous pressure (CVP) Noninvasive assessment JVD Hepatojugular reflux Peripheral edema * Weight* Left Preload Measured by the pulmonary artery occlusive pressure (PAOP) Noninvasive Assessment Lungs sounds Lymph drainage Blood pressure** Urine output / BUN/Creatinine Ratio** Weight* 9 10 Factors Influencing Preload Body Position Venous Tone Intrathoracic pressure Intrapericardial pressure Atrial Kick LV Function Circulating blood volume Hypervolemia Hypovolemia Third spacing Distribution of blood volume Sepsis Anaphylaxis Venous vasodilators Key Points about Preload Preload may need to be continuously balanced in cardiac patients Changes in pressure do not always = the same changes in volume Dilated versus noncompliant ventricle Heart failure does not mean congestion Right and left sided preload are closely related. Left heart preload is dependent on the right heart Associates 2

3 Afterload Afterload Pressure ventricle needs to overcome to eject blood volume Blood pressure is major component of afterload but it does not equal afterload Blood Pressure = Cardiac Output x Systemic Vascular Resistance (Afterload) Other components Valve compliance Viscosity of blood Arterial wall compliance Aortic compliance Right ventricular afterload Measured by pulmonary vascular resistance (PVR) Normal: dynes/sec/cm -5 Left ventricular afterload Measured by systemic vascular resistance (SVR) Normal dynes/sec/cm -5 Diastolic BP is closest noninvasive measurement (narrow pulse pressure) Causes of Increased LV Afterload Arterial vasoconstrictors Hypertension Aortic valve stenosis Increased blood viscosity Hypothermia Compensatory vasoconstriction from hypotension in shock Causes of Decreased LV Afterload Arterial vasodilators Hyperthermia Vasogenic shock states (sepsis and anaphylactic) where the body cannot compensate with vasoconstriction Aortic Regurgitation hyperdynamic cardiac output therefore lowering systemic vascular resistance 15 Increased Right Sided Afterload Pulmonary hypertension mpap > 25 mmhg or > 30 mmhg with exercise PVR > 250 dynes/sec/cm -5 Causes Hypoxemia Acidosis Inflammation Hypothermia Excess sympathetic stimulation Pulmonary endothelial dysfunction Impaired nitric oxide and prostacyclin (PGI2) release Primary pulmonary hypertension 16 Contractility Ability of myocardium to contract independent of preload or afterload Velocity and extent of myocardial fiber shortening Inotropic state Noninvasive Assessment: Ejection Fraction Contractility Related to degree of myocardial fiber stretch (preload) and wall tension (afterload). Influences myocardial oxygen consumption contractility myocardial workload myocardial oxygen consumption Associates 3

4 Contractility Measured on right by right ventricular stroke work index (5-12g-m/m 2 ) Measured on left by left ventricular stroke work index (45-65g-m/m 2 ) No ability to directly measure contractility. 19 Factors Altering Contractility Decreased contractility Excessive preload or afterload Drugs negative inotropes Myocardial damage Ischemia Cardiomyopathy Hypothyroidism Changes in ionic environment:hypoxia, acidosis or electrolyte imbalance Increased contractility Drugs Positive inotropes Hyperthyroidism Adrenal Medulla Tumor 20 Contractility Heart Rate Low cardiac output does not necessarily mean diminished contractility Correct preload and afterload problems first Inotropic Medication Sympathomimetics PDE Inhibitors Cardiac Glycosides Medications which increase contractility impact not only cardiac output but also myocardial oxygen demand. Mathematically heart rate increases cardiac output Physiological limit where increased heart rate will decrease cardiac output due to decreased filling time (decreased preload) Consider as first line strategy to increase cardiac output when temporary pacemaker in place Left Ventricular Function Curves Left Ventricular Function: Preload B A Associates 4

5 Left Ventricular Function: Contractility Left Ventricular Function: Afterload B B A A The Goal: Tissue Oxygenation Delivery of oxygen to the tissues is a function of cardiac output (or cardiac index) x arterial oxygen content Arterial oxygen content is impacted based on hemoglobin and arterial oxygenation saturation Delivery of oxygen = C.O. x Hgb X SaO 2 Poor oxygenation delivery can be improved by improving any of the above 3 parameters. Oxygen Delivery Always assess hemoglobin and oxygenation saturation in conjunction with cardiac performance Hypoxemia Ventilation Abnormalities PaCO 2 Rate and tidal volume Diffusion Barriers PaO2 and SaO 2 Oxygen and PEEP Oxygen Demand Critical illness can cause an increase in oxygen demand Surgery Pain Anxiety Infection Cellular Hypoxia Imbalance of supply and demand Cells unable to extract oxygen Result: Oxygen debt and anaerobic metabolism; eventual organ dysfunction Assessment: serum ph, lactate levels Associates 5

6 Other Factors Impacting Tissue Oxygenation Relationship between oxygen and hemoglobin (affinity) for proper uptake and unloading Temperature Hyperthermia Hypothermia ph Acidosis Alkalosis New StO 2 monitoring. Auscultatory Areas Utilization of Oxygenation By the Cells Cardiac Diastole (Atrial and Ventricular): Early Passive Filling Atrial Systole & Ventricular Diastole: Late Active Filling 33 Atrial Kick 34 Beginning Ventricular Systole: Isovolumic Contraction Ventricular Systole: Ejection Associates 6

7 FIRST HEART SOUND Basic Heart Sounds S 1 Closure of the Mitral (M 1 ) valve and the Tricuspid (T 1 )valve Beginning of Ventricular Systole and Atrial Diastole Isovolumic contraction Basic Heart Sounds S 1 Location: Mitral area at the hearts apex Intensity: Directly related to force of contraction Duration: Short Quality: Dull SECOND HEART SOUND Basic Heart Sounds S 2 Closure of Aortic (A 2 ) Valve and Pulmonic (P 2 ) Valve End of Ventricular Systole Beginning of Ventricular Diastole Basic Heart Sounds S 2 Location: Pulmonic area Intensity: Directly related to closing pressure in the aorta and pulmonary artery Duration: Shorter than S 1 Quality: Booming Associates 7

8 Third and Fourth Heart Sounds S 3 and S 4 Ventricular diastolic filling sounds Low frequency sounds Produced by ventricular filling rather than valve closure Normal in children and young adults THIRD HEART SOUND S 3 Ventricular Gallop Ventricular Gallop Early diastole Caused by increased diastolic pressure Left or Right Sided S 3 Left lateral position Location: Left Sided Mitral area Right Sided Tricuspid area Intensity: Left Sided Heard Best during expiration Right Sided Heard Best during inspiration Duration: Short Quality: dull, thudlike Pitch: Low S 4 Atrial Gallop S 4 Atrial Gallop Late diastole Caused by atrial contraction and the propulsion of blood into a noncompliant ventricle Associates 8

9 Left or Right Sided S 4 Left Lateral position Location: Left Sided Mitral Area Right Sided Tricuspid area Intensity: Left Sided Louder on expiration Right Sided Louder on inspiration Duration: Short Quality: Thudlike Pitch: Low Summation Gallop Combination of S3 and S MURMURS Murmur Fundamentals Turbulence Murmur: If turbulence is intracardiac Bruit: If turbulence is extracardiac Murmur Fundamentals Causes of Turbulence Forward flow through a stenotic valve Murmur Fundamentals Causes of Turbulence Flow through a septal defect or an AV fistula Backward flow through an incompetent valve Flow into a dilated chamber or a portion of a vessel Associates 9

10 Murmur Fundamentals Murmur Fundamentals Stenotic Murmurs Valve does not open appropriately Heard during the part of the cardiac cycle when the valve is open Regurgitant Murmurs Valve does not close appropriately Heard during the part of the cardiac cycle when the valve is to be closed Timing Systolic Holosystolic Ejection (midsystolic) Late Diastolic Early Middiastolic Late Location Place heard the loudest Radiation Direction in which murmur radiates Murmur Fundamentals Systolic Murmurs Configuration Crescendo Gets louder Decrescendo Gets softer Crescendo Decrescendo Louder then softer Plateau Even intensity throughout Pitch High Pitched - diaphragm Low Pitched bell Quality Soft Harsh Blowing Musical Rumbling Rough Tricuspid and Mitral Valve Closed Tricuspid Regurgitation Mitral Regurgitation Pulmonic and Aortic Valve Open Pulmonic Stenosis Aortic Stenosis Aortic Stenosis Systolic Ejection Murmur Timing: Midsystolic Location: Best heard over aortic area Radiation: Toward right side of neck Crescendo-decrescendo Pitch: Medium to high Quality: Harsh Pulmonic Stenosis Systolic Ejection Murmur Timing: Midsystolic Location: Best heard over pulmonic area Radiation: Left neck of left shoulder Crescendo-decrescendo Pitch: Medium Quality: Harsh Associates 10

11 Systolic Murmurs Mitral Regurgitation Timing: Holosystolic Location: Mitral area Radiation: To the left axilla Plateau Quality: Blowing, harsh or musical Systolic Murmurs Tricuspid Regurgitation Timing: Holosystolic Location: Tricuspid area Radiation: To the right of sternum Plateau Quality: Scratchy or blowing Diastolic Murmurs Diastolic regurgitant murmurs Retrograde flow across an incompetent semilunar valve Diastolic filling murmurs Forward flow across stenotic or obstructed AV valves Diastolic Murmurs Tricuspid and Mitral Valves Open Tricuspid Stenosis Mitral Stenosis Pulmonic and Aortic Valves Close Pulmonic Regurgitation Aortic Regurgitation Diastolic Murmurs Aortic Regurgitation Timing: Early diastole Location: Aortic area Radiation: Toward apex Decrescendo Quality: Blowing Diastolic Murmurs Pulmonic Regurgitation Timing: Early diastole Location: Pulmonic area Erb s Point Radiation: Toward apex Decrescendo Quality: Blowing Associates 11

12 Diastolic Murmurs Mitral Stenosis Diastolic Murmur Tricuspid Stenosis Timing: Mid to Late diastole Location: Mitral area Radiation: None Crescendo Pitch: Low Quality: Rumbling 67 Timing: Mid to Late diastole Location: Tricuspid area Radiation: None Decrescendo Pitch: Low Quality: Rumbling Increases during inspiration and decreases during expiration 68 Other Sounds Pericardial Friction Rub Timing: Systolic, Early diastolic and late diastolic Location: Tricuspid area and Xyphoid area Radiation: None Plateau May get louder during inspiration Quality: Grating, scratching Other Sounds Ventricular Septal Defect or Rupture Timing: Continuous Location: 3-4 LSB Radiation: Widely throughout the precordium Plateau Quality: Harsh Other Sounds REMEMBER: Papillary Muscle Rupture Same as Mitral Regurgitation The most important part of the stethoscope is the part between the ear pieces Associates 12

13 JVP (Jugular Venous Pressure) Other Assessment Tools Reflects volume and pressure in right side of heart Visual inspection HOB degree angle 45 degree angle will cause venous pulsation to rise 1 to 3 cm above the manubrium Measuring JVD Raise HOB until pulsation in internal jugular seen (usually degrees) Use targeted light Use centimeter ruler Measure distance from angle of Louis (Manubriosternal joint) to top column of blood Draw imaginary horizontal line from column to sternal angle JVD (Jugular Venous Distension) Normal JVD level is 3 cm above the sternal angle Sternal angle is 5cm above right atrium JVD of 3 cm + 5cm = estimated CVP of 8cm Estimated CVP> 8 cm Increased blood volume Usually RV failure Tricuspid valve regurgitation Pulmonary hypertension Tips to Take Away for JVD Assessment If unable to accurately assess Lie patient flat to visualize and then raise HOB If venous congestion is expected may need to sit or stand patient to see top of column No Low Perfusion CI 2.2 at Rest Profiles of Perfusion and Congestion Yes Congestion at Rest No Yes Warm and Dry Warm and Wet No congestion Congestion No hypoperfusion No hypoperfusion Cold and Dry No congestion Hypoperfusion PWP 18 Cold and Wet Congestion Hypoperfusion Associates 13

14 Cardiac Assessment Arterial vs. Venous Disease Edema Evaluated on a 4-point scale. 0 = None present. 1+ = 0 to 1 4 inch Trace. 2+ = 1 4 to 1 2 inch Mild. 3+ = 1 2 to 1 inch Moderate. 4+ = > than 1 inch Severe. Described as pitting or non-pitting. Anasarca: generalized edema Pulses 4 point scale (0-3) 0 = absent 1+ = Palpable but thready and weak, easily obliterated 2+ = Normal, easily identified, not easily obliterated 3+ = Full, bounding, cannot obliterate Central Cyanosis Occurs when more than 5 grams/dl of hemoglobin is deoxygenated Results in a bluish or steel-gray discoloration of the skin and mucous membranes Bluish or steel-gray discoloration of the lips can be from central or peripheral cyanosis Oral mucosa or the tongue may be better tools for assessment of central cyanosis Usually not seen until oxygen saturation drops to between 73% to 78% Absence of cyanosis does not exclude hypoxemia Peripheral Cyanosis Caused by peripheral vasoconstriction and decreased local blood flow May occur with or without central cyanosis (i.e., with or without hypoxemia) Usually observed in the nailbeds of the hands or feet, the earlobes or nose Should improve with warming 83 Pulsus Paradoxus To measure the pulsus paradoxus, patients are often placed in a semirecumbent position; respirations should be normal. The blood pressure cuff is inflated to at least 20 mm Hg above the systolic pressure and slowly deflated until the first Korotkoff sounds are heard only during expiration. At this pressure reading, if the cuff is not further deflated and a pulsus paradoxus is present, the first Korotkoff sound is not audible during inspiration. As the cuff is further deflated, the point at which the first Korotkoff sound is audible during both inspiration and expiration is recorded. If the difference between the first and second measurement is greater than 12 mm Hg, an abnormal pulsus paradoxus is present. (Yarlagadda, Chakri, 2005 Cardiac Tamponade. Retrieved from 84 Associates 14

15 Blood Pressure Definitions: BP = CO X SVR Systolic: Maximum pressure when blood is expelled from the left ventricle Diastolic:Measures rate of flow of ejected blood and vessel elasticity Pulse Pressure: Difference between systolic and diastolic pressure Clinical Significance Blood Pressure Control Rapid adjustments in BP are controlled by baroreceptor reflexes Baroreceptor reflex is sluggish with orthostatic hypotension Additional mechanisms for blood pressure control Nerve fibers: limbic system and hypothalamus (emotionally triggered) Neural input from midbrain (pain) Chemoreceptors: Hypercapnia and hypoxia Calcium: Vascular tone and contractility Renin angiotensin aldosterone system (RAAS) Vasopressin (Antidiuretic hormone) Endothelial response Etiology of Hypotension Blood pressure does not equal blood flow. BP 88/72 CO SVR BP CO SVR 82/ Gratitude 89 Associates 15