Brent Dunworth, CRNA, MSN, MBA Associate Director of Advanced Practice Division Chief, Nurse Anesthesia Vanderbilt University Medical Center Nashville, Tennessee Learning Objectives Review the principles of the cardiovascular system as they relate to the effects of anesthetic drugs. Describe the cardiovascular anatomy, physiology, and pathophysiology. Describe the impact of selection of pharmacologic agents on patient comorbidity. 2 Continuous Professional Recertification Crosswalk to Examination Preparation Domain II: Applied Clinical (24%) II.A. Pharmacokinetics/pharmacodynamics/Pharmacogenetics of anesthetics and adjunct medications II.B. Factors influencing medication selection II. B.1. Physiological II. B.2. Pathophysiological II. B.3. Laboratory & diagnostic studies II. B.4. Utilization, actions, interactions, benefits, adverse effects, abnormal responses, alternatives, and antagonists II. B.5. Comorbidity II.C. Intraoperative monitoring techniques II.D. Infection prevention principles II.E. Adverse Pharmacological Reactions Domain III: Human Physiology and Pathophysiology (24%) III.A. Cardiovascular III. A.1. Normal anatomical structures and function III. A.2. Physiologic processes and anesthetic considerations III. A.3. Pathophysiologic disease processes and associated disorders 3 Brent Dunworth, CRNA, MSN, MBA 1
Physiology Concepts Pressure-Volume Curves Physiologic Changes Pathophysiologic Changes 4 Determinants of Ventricular Performance Systolic function Ventricular ejection Diastolic function Ventricular filling Equated with CO CO=HR x SV 5 Ventricular Performance Heart Rate CO generally proportional Stroke Volume Preload Afterload Contractility 6 Brent Dunworth, CRNA, MSN, MBA 2
Preload End diastolic volume Dependent on ventricular filling Starling Law Relationship between CO and LVEDV 7 Determinants of Ventricular Filling Venous return Blood volume Distribution of blood volume Posture Intrathoracic pressure Pericardial pressure Venous tone Rhythm Heart Rate 8 Starling Law 9 Brent Dunworth, CRNA, MSN, MBA 3
Ventricular Compliance 10 Ventricular Compliance Early diastolic compliance reduction Hypertrophy Ischemia Asynchrony Late diastolic compliance reduction Hypertrophy Fibrosis 11 Ventricular Compliance Extrinsic factors Pericardial disease Overdistention of contralateral ventricle Pleural pressure Tumors Surgical compression 12 Brent Dunworth, CRNA, MSN, MBA 4
Ventricular Compliance 13 Afterload Ventricular wall tension during systole Law of LaPlace Larger radius greater wall tension required to develop the same pressure 14 Law of LaPlace 15 Brent Dunworth, CRNA, MSN, MBA 5
Law of LaPlace 16 Afterload Arterial impedance to ejection SVR Arteriolar tone 17 Afterload 18 Brent Dunworth, CRNA, MSN, MBA 6
Afterload 19 Contractility Intrinsic ability to pump in the absence of changes in preload or afterload Dependent on intracellular calcium concentration during systole 20 Valvular Dysfunction Stenosis AV valve (tricuspid, mitral) Reduced stroke volume primarily by decreasing ventricular preload Semilunar valve (pulmonary, aortic) Reduced stroke volume by increased afterload 21 Brent Dunworth, CRNA, MSN, MBA 7
Valvular Dysfunction Insufficiency (regurgitation) Reduced stroke volume due to regurgitant volume with every contraction EDV can flow backward into atrium (or ventricle) during systole Effective (forward) stroke volume decreased 22 Physiology Concepts Pressure-Volume Curves Physiologic Changes Pathophysiologic Changes 23 Cardiac Cycle 24 Brent Dunworth, CRNA, MSN, MBA 8
Diastole: Filling 25 Atrial Contraction 26 Systole: Isovolumetric Contraction 27 Brent Dunworth, CRNA, MSN, MBA 9
Systole: Ejection 28 Diastole: Isovolumetric Relaxation 29 Diastole: Ventricular Filling 30 Brent Dunworth, CRNA, MSN, MBA 10
Systole: Isovolumetric Contraction ED 31 Systole: Ejection ED 32 Diastole: Isovolumetric Relaxation ES. ED 33 Brent Dunworth, CRNA, MSN, MBA 11
Key Points A mitral valve opens ventricular filling B EDV ventricular contraction begins systole C AV opens ejection D AV closes ESV isovolumetric relaxation diastole 34 Physiology Concepts Pressure-Volume Curves Physiologic Changes Pathophysiologic Changes 35 Changes in Preload Physiologic Change Preload End diastolic stress on ventricle End diastolic fiber length End diastolic volume 36 Brent Dunworth, CRNA, MSN, MBA 12
Preload Concepts When preload increases, EDV (filling) increases Preload decreases, EDV decreases Ventricle empties to the same point (same ESV); stoke volume changes 37 Increased Preload ESV 38 Preload Reduction 39 Brent Dunworth, CRNA, MSN, MBA 13
Afterload Concepts When afterload increases; the ventricle empties less completely SV (EDV-ESV) decreases BP increases (shown as increased LV pressure as ejection begins) 40 Afterload Concepts When afterload decreases, the ventricle empties more completely. SV (EDV-ESV) increases Decreased BP (decreased LV pressure at ejection) 41 Changes in Afterload Physiologic Increased Increased pressure and Volume Decreased Smaller pressures and volumes 42 Brent Dunworth, CRNA, MSN, MBA 14
Increased Afterload 43 Afterload Reduction 44 Changes in Heart Rate CO = HR x SV 45 Brent Dunworth, CRNA, MSN, MBA 15
Contractility Concepts Increase (digitalis, calcium) Ventricle empties more completely ESV and EDV decrease ( shrinks ) SV increases BP increases Decrease (heart failure) Ventricle empties less completely ESV and EDV increase ( dilates ) SV, BP decrease 46 Contractility Changes Preload and afterload are constant Increase: higher pressure and smaller volumes Decrease: lower pressure; higher volumes 47 Physiology Concepts Pressure-Volume Curves Physiologic Changes Pathophysiologic Changes 48 Brent Dunworth, CRNA, MSN, MBA 16
Valvular Pathology Aortic Valve Insufficiency Acute Chronic Stenosis Mitral Valve Insufficiency Stenosis Hypertrophic Cardiomyopathy 49 Aortic Insufficiency 50 Aortic Insufficiency Etiologies Abnormalities of the Leaflets Rheumatic, Bicuspid, Degenerative Endocarditis Dilation of the Aortic Annulus Aortic Aneurysm / Dissection Inflammatory Syphilis Giant Cell Arteritis Collagen Vascular Disease Ankylosis Spondylitis Inherited Marfans Osteogensis Imperfecta 51 Brent Dunworth, CRNA, MSN, MBA 17
Aortic Insufficiency 52 Aortic Insufficiency Acute Chronic Blood regurgitated into LV during diastole 53 Acute vs. Chronic AI Eccentric Hypertrophy 54 Brent Dunworth, CRNA, MSN, MBA 18
Management of AI Parameter Preload Afterload Rate Contractility Oxygen balance Goal Rhythm Sinus Fast, full, forward Maintain preload Decrease; vasodilator beneficial Prevent slow rate (<80 bpm) Decreased in chronic Increased demand as a result of increase in LV mass 55 Aortic Stenosis 56 Aortic Stenosis Etiology & Incidence 38% Congenital bicuspid 33% Degenerative calcification 24% Postinflammatory fibrocalcific (Rheumatic Heart Disease) 2% Unicommissural aortic valve 1% Hypoplastic 57 Brent Dunworth, CRNA, MSN, MBA 19
Aortic Stenosis Pathophysiology Compensatory Changes 58 Bicuspid Aortic Valve 59 Aortic Stenosis: Progression Symptom Cause Median Survival Angina Elevated LVEDP decreases perfusion pressure 5 years Myocardial hypertrophy increases demand Syncope Inability to increase CO and meet reduced SVR demands Heart Failure Elevated LVEDP elevated LA pressure pulmonary venous congestion 3 years 2 years 60 Brent Dunworth, CRNA, MSN, MBA 20
AVA: Rate of Flow vs. Systolic Pressure 61 Aortic Stenosis About same LV volume; much greater pressure 62 Management of AS Parameter Preload Afterload Rate Contractility Oxygen balance Rhythm Goal Increase to distend the stiff ventricle Decrease is hazardous Normal to Slow (increase in rate can produce ischemia) Decreased to normal Increased demand as a result of increase in LV mass Sinus 63 Brent Dunworth, CRNA, MSN, MBA 21
Mitral Regurgitation 64 Mitral Regurgitation Etiologies Alterations of the Leaflets, Commissures, Annulus Rheumatic MVP Endocarditis Alterations of LV or LA size and Function Papillary Muscle (Ischemic, MI, Myocarditis, DCM) HOCM LV Enlargement Cardiomyopathies LA Enlargement from MR MR begets MR 65 Mitral Regurgitation Decreased ventricular volume during isovolumetric contraction 66 Brent Dunworth, CRNA, MSN, MBA 22
Mitral Regurgitation Increased LV emptying; retrograde flow into LA 67 Management of MR Parameter Preload Afterload Rate Contractility Oxygen balance Rhythm Goal Normal to increased Decreased, vasodilator beneficial Prevent slow rate (<80 bpm) Decreased from rheumatic or coronary artery disease increased demand as a result of increased mass Sinus Atrial fibrillation tolerated if rate is controlled 68 Mitral Stenosis 69 Brent Dunworth, CRNA, MSN, MBA 23
Mitral Stenosis Etiology 99% 1% postinflammatory (Rheumatic) congenital Pathophysiology LA hypertension Pulmonary interstitial edema Pulmonary hypertension LA stretch and atrial fibrillation Limited LV filling and cardiac output 70 Mitral Stenosis Symptoms Dyspnea Pulmonary venous congestion Fatigue Diminished cardiac output Inability to tolerate volume Inability to tolerate increased HR Decreased filling Increased LA pressure / PV congestion Hemoptysis 71 Mitral Stenosis Less LV filling 72 Brent Dunworth, CRNA, MSN, MBA 24
Management of MS Parameter Preload Afterload Rate Contractility Oxygen balance Rhythm Goal Normal to increased Maintain; increase is poorly tolerated About 80 bpm; tachycardia and bradycardia decrease CO Normal Normal Sinus Atrial fibrillation tolerated if ventricular rate <80 bpm 73 Hypertrophic Obstructive Cardiomyopathy (HOCM) 74 Hypertrophic Cardiomyopathy Etiology No identifiable cause Evidence of myocardial fiber disarray Treatment Medical management Surgical myomectomy 75 Brent Dunworth, CRNA, MSN, MBA 25
Hypertrophic Cardiomyopathy P P Chamber gets small Small volume High Pressure V 76 Management of Hypertrophic Cardiomyopathy Parameter Preload Afterload Rate Contractility Oxygen balance Rhythm Goal Normal to high High Rate <80 bpm Decreased Increased demand as a result of increased LV mass Sinus rhythm 77 Physiology Concepts Pressure-Volume Curves Physiologic Changes Pathophysiologic Changes 78 Brent Dunworth, CRNA, MSN, MBA 26
Causes of Hypotension Hypovolemia Hemorrhage Dehydration Blood volume redistribution Postural changes Reduced cardiac output Acute heart failure Chronic heart failure Reduced systemic vascular resistance Loss of sympathetic tone Vasodilation (septic shock, anaphylaxis) http://www.cvpharmacology.com/clinical%20topics/hypotension 79 Treatment of Hypotension GOAL: RAISE ARTERIAL BLOOD PRESSURE Increase cardiac output Increase blood volume Stimulate contractility Increase systemic vascular resistance Vasoconstrictor drugs http://www.cvpharmacology.com/clinical%20topics/hypotension-2 80 Contractility Sympathomimetic Stimulate heart (beta receptors) Vascular smooth muscle contraction (alpha receptors) Side effects Increase in myocardial oxygen demand Cardiac arrhythmia Angina, ischemia http://www.cvpharmacology.com/cardiostimulatory/beta-agonist 81 Brent Dunworth, CRNA, MSN, MBA 27
Contractility http://www.cvpharmacology.com/cardiostimulatory/beta-agonist Drug Receptor Selectivity Clinical Use Comments Epinephrine Norepinephrine Dopamine β 1 = β 2 > α 1* = α 2* *At high plasma concentrations, α = β selectivity. β 1 = α 1 > β 2 = α 2 β 1 = β 2 > α 1* *At low doses, it stimulates the heart and decreases systemic vascular resistance; at high doses, vasodilation becomes vasoconstriction as lower affinity α- receptors bind to the dopamine; also binds to D1 receptors in kidney, producing vasodilation. Anaphylactic shock; cardiogenic shock; cardiac arrest Severe hypotension; septic shock Acute heart failure, cardiogenic shock and acute renal failure Dobutamine β 1 > β 2 > α 1 Acute heart failure; cardiogenic shock; refractory heart failure Isoproterenol β 1 = β 2 Bradycardia and atrioventricular block Low doses produce cardiac stimulation and vasodilation, which turns to vasoconstriction at high doses. Reflex bradycardia masks direct stimulatory effects on sinoatrial node. Biosynthetic precursor of norepinephrine; stimulates norepinephrine release. Net effect is cardiac stimulation with modest vasodilation. Net effect is cardiac stimulation and vasodilation with little change in pressure. 82 Alpha agonists Phenylephrine Side effects Reflex bradycardia Increase afterload (increased myocardial workload) Angina, ischemia http://www.cvpharmacology.com/vasoconstrictor/alpha-agonist 83 Vasopressin Potent vasoconstrictor (V 1 receptor) Side effects Bronchoconstriction Water intoxication, hyponatremia Increases myocardial oxygen demand (increased afterload) Coronary artery constrictor http://www.cvpharmacology.com/vasoconstrictor/avp 84 Brent Dunworth, CRNA, MSN, MBA 28
Phosphodiesterase inhibitors Phosphodiesterase breaks down camp camp is an important second messenger in cardiac muscle contraction Breakdown prevention increases cardiac inotropy, chronotropy, and dromotropy (conduction velocity). Systemic circulation Vasodilation Increased organ perfusion Decreased SVR Decreased arterial pressure Cardiopulmonary increased contractility and rate increased stroke volume and EF decreased ventricular preload decreased PCWP http://www.cvpharmacology.com/vasodilator/pdei 85 Clinical Decision Making 86 Brent Dunworth, CRNA, MSN, MBA 29