Advanced Cardiac Dynamics Presented by: Karen Marzlin BSN, RN, CCRN-CMC CNEA 2009 1 Hemodynamics does not equal invasive monitoring Paradigm Shift 2 www.cardionursing.com 1
3 Circulation: Heart Arteries Veins Blood Volume 4 www.cardionursing.com 2
Layers of Arteries Intima Endothelium Decreases resistance Minimizes platelet aggregation Media Changes in diameter BP Adventitia Fibrous outer layer Connection to structure Arteries Plaque forms between the intima and media 5 Endothelial Function Response to atherosclerotic plaque Angiotensin II Increases oxidative stress Decrease nitric oxide Increase endothelin CRP Inflammation Flow mediated endothelium dependent vasomotion Ultrasound brachial artery Acetycholine infusion 6 www.cardionursing.com 3
Layers of Veins Intima Media Adventitia Valves Veins 7 Neurological Impact on Circulation and Hemodynamics 8 www.cardionursing.com 4
Neurologic Control Autonomic Nervous System SNS PNS Baroreceptors 9 Autonomic Nervous System Both divisions of the autonomic nervous system extend into the heart The atria are innervated by both parasympathetic and sympathetic fibers (SA node and AV node) The ventricles are innervated by sympathetic fibers only (myocardial tissue) 10 www.cardionursing.com 5
Sympathetic Nervous System (SNS) SNS (adrenergic) Neurotransmitters: Epinephrine and Norepinephrine Fight or flight + chronotropic + dromotropic + inotropic Alpha, Beta 1, Beta 2 and Dopamanergic receptors 11 Sympathetic Nervous System (SNS): Receptor Sites Alpha 1 Vasoconstriction of vessels Beta 1 Increase heart rate, contractility, conductivity Beta 2 Bronchodilitation, vasodilatation Dopamanergic Dilatation of renal and mesenteric arteries 12 www.cardionursing.com 6
Parasympathetic Nervous System (PNS) PNS (Vagal) (Cholinergic) Neurotransmitter: Acetylcholine Maintains a steady state Causes decrease in chronotropic and dromotropic effects Causes minimal decrease in inotropic effects New area of research in heart failure 13 Baroreceptors Located in the carotid sinus and aortic arch (sensitive to arterial wall tension) Two reflexes control release of adrenergic (SNS) or cholinergic (PNS) neurotransmitters Aortic Reflex Bainbridge Reflex 14 www.cardionursing.com 7
Aortic and Bainbridge Reflexes Aortic Increase in arterial BP Stimulate aortic and carotid sinus baroreceptors Parasympathetic (vagal) discharge from medulla Decrease in HR and CO therefore decrease in BP Bainbridge Increase in venous BP Stimulates vena cava baroreceptors Increase sympathetic discharge and decreased parasympathetic discharge Increase in HR to handle increase in venous return 15 Renin-angiotensin System Renal Blood Flow Renin Release Angiotensinogen Angiotensin I Angiotension II (Converting Enzyme) Vasoconstriction Aldosterone Release Na and H2O Retention BP 16 www.cardionursing.com 8
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 17 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 18 www.cardionursing.com 9
Blood pressure does not equal blood flow. 19 Valve Abnormalities : Effect on Hemodynamics Stenosis Impedes the forward flow of blood Regurgitation Insufficiency, Incompetent Allows backward flow of blood 20 www.cardionursing.com 10
The Cardiac Cycle Systole and Diastole 21 Diastole (atrial and ventricular): Early Passive Filling 22 www.cardionursing.com 11
Atrial Systole (atrial kick) & Ventricular Diastole: Late Active Filling 23 Beginning Ventricular Systole: Isovolumic Contraction 24 www.cardionursing.com 12
Ventricular Systole: Ejection 25 Regulation of Fluid Balance Fluid intake Hormonal Control Antidiuretic hormone Aldosterone Fluid Output 26 www.cardionursing.com 13
Fluid Intake Fluid intake is regulated by the thirst mechanism 1. Osmoreceptors in the hypothalmus are stimulated by an increase in osmotic pressure of body fluids and will stimulate thirst 2. Osmoreceptors are also stimulated by a decrease in extracellular fluid volume 3. A decrease in salivary secretions from certain medications (example atropine) will also stimulate thirst Clinical Implication: Those patients unable to communicate thirst need to be offered frequent opportunities for hydration. 27 Hormonal Control Antidiuretic Hormone Posterior lobe of pituitary gland Water conservation hormone Aldosterone Adrenal Cortex Regulates extracellular fluid volume by increasing reabsorption of sodium and chloride (and water) 28 www.cardionursing.com 14
A Closer Look at Antidiuretic Hormone Regulates the osmotic pressure of extracellular fluid by regulating the amount of water reabsorbed in the renal tubules ADH release is stimulated by an increase in osmotic pressure increased ADH causes dilution of blood attempting to return osmotic pressure to normal Excreted urine volume will be decreased and the concentration of urine will be increased 29 A Closer Look at Aldosterone Aldosterone primarily works on sodium retention and water retention follows Aldosterone promotes excretion of potassium and hydrogen Aldosterone production is increased in healthy persons: Low fluid volume Low blood sodium High blood potassium 30 www.cardionursing.com 15
A Closer Look at Aldosterone Diseases causing over production of aldosterone Cushing s Syndrome Diseases causing under production of aldosterone Adrenalectomy Aids Metastatic Cancer 31 Fluid Output Change in extracellular fluid result in change in intravascular volume change in venous return to the heart and cardiac output change in arterial pressure sensed by the kidneys change in fluid excretion by the kidneys Fluid is also lost through: GI Tract Skin Lungs 32 www.cardionursing.com 16
Body Fluid Compartments Intracellular Inside the cells 40% of adult body weight Extracellular Outside the cells 20% of adult body weight Intravascular Interstitial 33 More About Extracellular Fluid Intravascular Fluids within the blood vessels Interstitial Fluid between the blood vessels and cells Intravascular and interstitial fluids are not static as they move through capillary walls. 34 www.cardionursing.com 17
Movement of Fluid and Electrolytes Capillary Permeability Diffusion Osmosis Filtration Active Transport Hydrostatic Pressure Colloidal Osmotic Pressure 35 Extracellular Fluid Volume Deficit Extracellular fluid volume deficit Remaining fluid is more concentrate (hypertonic) Fluid moves out of cells (cellular dehydration) 36 www.cardionursing.com 18
Extracellular Fluid Volume Deficit Elderly at risk Decrease in total body water Reduced sense of thirst Reduced ability of kidneys to concentrate urine Also at risk: infants, those with burns or infections 37 Extracellular Fluid Volume Deficit Diagnostic Lab Values Elevated hematocrit Proportion of erythrocytes to blood plasma Normal 35 to 45% women 40 to 50% men Hematocrit is elevated due to hemoconcentration Elevated sodium (hyperosmolar hypernatremia) Increased urine specific gravity 38 www.cardionursing.com 19
Extracellular Fluid Volume Overload Does not occur as primary problem unless compensatory mechanisms fail Normal compensation Excess ECF Water moves into cells Osmoreceptors respond Decrease ADH Increased urine output 39 Extracellular Fluid Volume Overload Kidney disease Decreased cardiac output Excessive ADH Fear Pain Acute Infection Analgesics Trauma Acute Stress 40 www.cardionursing.com 20
Extracellular Fluid Volume Overload Extracellular fluid volume excess Decreased oncotic pressure Fluid moves into cells Cellular swelling 41 Fluid Shifting Large quantities of fluid shift from intravascular to extravascular space Increased capillary permeability allowing plasma protein to leak into interstitial spaces Decreased intravascular oncotic pressure Lymphatic blockage Can be general or localized 42 www.cardionursing.com 21
Phases of Fluid Shifting Phase I Fluid shifts out of vascular space and symptoms resemble fluid volume deficit (circulating volume is decreased) Phase II Fluid is reabsorbed and moves back into vascular space Process occurs gradually and does not cause signs of fluid overload 43 Crystalloid IV Solutions Hypotonic Isotonic Hypertonic Lower concentration of salt or more water than isotonic Causes movement of fluids into cells.45 NS or D5W Like human cells or intracellular fluid Very little osmosis.9ns or LR Higher concentration of salt or less water than isotonic Pulls fluid out of cells 3% NS 44 www.cardionursing.com 22
Colloid Solutions Colloids contain particles not capable of passing through semi permeable membrane They are retained in the vascular system They increase oncotic pressure Fluid is drawn into the vascular space Circulating volume is increased. Crystalloids contain substances that can diffuse through semi permeable membranes 45 Hemodynamics: Cardiac Output Understanding basic hemodynamic principles and their impact on the forward propulsion of blood. 46 www.cardionursing.com 23
Basic Hemodynamic Formula Cardiac Output Heart Rate X Stroke Volume Preload Afterload Contractility Stroke Volume: Volume of blood ejected with each beat 60-120 ml/beat 47 Cardiac Output 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: 60-120 ml/beat Ejection Fraction: Percent of blood ejected from the ventricle 48 Normal: 55%-60% www.cardionursing.com 24
Right Sided vs. Left Side System 49 Preload End-diastolic 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 50 www.cardionursing.com 25
Right and Left Sided Preload 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* 51 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 52 www.cardionursing.com 26
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. 53 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 54 www.cardionursing.com 27
Afterload Right ventricular afterload Measured by pulmonary vascular resistance (PVR) Normal: 150-250 dynes/sec/cm -5 Left ventricular afterload Measured by systemic vascular resistance (SVR) Normal 900-1200 dynes/sec/cm -5 Diastolic BP is closest noninvasive measurement (narrow pulse pressure) 55 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 56 www.cardionursing.com 28
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 (PGI 2 ) release Primary pulmonary hypertension 57 Contractility Ability of myocardium to contract independent of preload or afterload Velocity and extent of myocardial fiber shortening Inotropic state Noninvasive Assessment: Ejection Fraction 58 www.cardionursing.com 29
Contractility Related to degree of myocardial fiber stretch (preload) and wall tension (afterload). Influences myocardial oxygen consumption contractility myocardial workload myocardial oxygen consumption 59 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 65g-m/m 2 ) No ability to directly measure contractility. 60 www.cardionursing.com 30
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 61 Contractility Low cardiac output does not necessarily mean diminished contractility Correct preload and afterload problems first Medications which increase contractility impact not only cardiac output but also myocardial oxygen demand. Inotropic Medication Sympathomimetics PDE Inhibitors Cardiac Glycosides 62 www.cardionursing.com 31
Heart Rate 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 63 Left Ventricular Function Curves 64 www.cardionursing.com 32
Left Ventricular Function: Preload A B 65 Left Ventricular Function: Contractility B A 66 www.cardionursing.com 33
Left Ventricular Function: Afterload B A 67 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. 68 www.cardionursing.com 34
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 69 Oxygen Demand Critical illness can cause an increase in oxygen demand Surgery Pain Anxiety Infection 70 www.cardionursing.com 35
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 71 Assessing Supply and Demand Invasive: Venous oxygen saturation Noninvasive: Organ function Mentation Urine Output 72 www.cardionursing.com 36
Other Factors Impacting Tissue Oxygenation Relationship between oxygen and hemoglobin (affinity) for proper uptake and unloading Temperature Temperature Hyperthermia Hypothermia ph Acidosis Alkalosis New StO 2 monitoring. Utilization of Oxygenation By the Cells 73 Thanks for Attending Cardiovascular Boot Camp You may contact us at www.cardionursing.com 74 www.cardionursing.com 37
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